PMID- 30786044
OWN - NLM
STAT- In-Data-Review
LR  - 20190405
IS  - 1531-8249 (Electronic)
IS  - 0364-5134 (Linking)
VI  - 85
IP  - 4
DP  - 2019 Apr
TI  - Concordance for Parkinson's disease in twins: A 20-year update.
PG  - 600-605
LID - 10.1002/ana.25441 [doi]
AB  - During the 1990s, we estimated the genetic contribution to Parkinson's disease
      risk in a large, population-based twin registry. Because many unaffected twins
      were still alive, previous concordance estimates were based on incomplete
      information. Ninety-five percent of twins are now deceased. Here, we update
      concordance and heritability through 2015 using National Death Index data. In
      total, we identified 30 concordant and 193 discordant pairs. Proband-wise
      concordance was 0.20 in monozygotic and 0.13 in dizygotic pairs. Heritability was
      0.27 overall, 0.83 in pairs diagnosed </=50, and 0.19 in pairs diagnosed >50.
      High concordance in dizygotic twins suggests shared effects of early childhood
      environment. Ann Neurol 2019;85:600-605.
CI  - (c) 2019 American Neurological Association.
FAU - Goldman, Samuel M
AU  - Goldman SM
AD  - Division of Occupational and Environmental Medicine; University of California-San
      Francisco, San Francisco Veterans Affairs Health Care System, University of
      California-San Francisco, San Francisco, CA.
FAU - Marek, Kenneth
AU  - Marek K
AD  - Institute for Neurodegenerative Disorders, New Haven, CT.
FAU - Ottman, Ruth
AU  - Ottman R
AD  - G.H. Sergievsky Center, Columbia University, New York, NY.
FAU - Meng, Cheryl
AU  - Meng C
AD  - Department of Neurology, University of California-San Francisco, San Francisco,
      CA.
FAU - Comyns, Kathleen
AU  - Comyns K
AD  - Department of Neurology, University of California-San Francisco, San Francisco,
      CA.
FAU - Chan, Piu
AU  - Chan P
AD  - Department of Neurobiology and Neurology; National Clinical Research Center for
      Geriatric Disorders, Xuanwu Hospital of Capital Medical University, Beijing,
      China.
FAU - Ma, Jinghong
AU  - Ma J
AD  - Department of Neurology, Xuanwu Hospital of Capital Medical University, Beijing, 
      China.
FAU - Marras, Connie
AU  - Marras C
AD  - Department of Neurology, Toronto Western Hospital, University of Toronto,
      Toronto, Ontario, Canada.
FAU - Langston, J William
AU  - Langston JW
AD  - Department of Pathology, Stanford University, Palo Alto, CA.
FAU - Ross, G Webster
AU  - Ross GW
AD  - VA Pacific Islands Health Care System; Pacific Health Research and Education
      Institute, Honolulu, HI.
FAU - Tanner, Caroline M
AU  - Tanner CM
AD  - Department of Neurology; University of California-San Francisco, San Francisco
      Veterans Affairs Health Care System, University of California-San Francisco, San 
      Francisco, CA.
LA  - eng
GR  - RO1-NS40467/National Institute of Neurological Disorders and Stroke
GR  - U10-NS31321/National Institute of Neurological Disorders and Stroke
GR  - UCSF Academic Senate Committee on Research
PT  - Journal Article
DEP - 20190311
PL  - United States
TA  - Ann Neurol
JT  - Annals of neurology
JID - 7707449
EDAT- 2019/02/21 06:00
MHDA- 2019/02/21 06:00
CRDT- 2019/02/21 06:00
PHST- 2018/09/06 00:00 [received]
PHST- 2019/02/18 00:00 [revised]
PHST- 2019/02/18 00:00 [accepted]
PHST- 2019/02/21 06:00 [pubmed]
PHST- 2019/02/21 06:00 [medline]
PHST- 2019/02/21 06:00 [entrez]
AID - 10.1002/ana.25441 [doi]
PST - ppublish
SO  - Ann Neurol. 2019 Apr;85(4):600-605. doi: 10.1002/ana.25441. Epub 2019 Mar 11.

PMID- 30776897
OWN - NLM
STAT- In-Data-Review
LR  - 20190219
IS  - 1520-4995 (Electronic)
IS  - 0006-2960 (Linking)
VI  - 58
IP  - 7
DP  - 2019 Feb 19
TI  - A PARP-1 Feed-Forward Mechanism To Accelerate alpha-Synuclein Toxicity in
      Parkinson's Disease.
PG  - 859-860
LID - 10.1021/acs.biochem.8b01311 [doi]
FAU - Pan, Buyan
AU  - Pan B
AD  - Department of Chemistry , University of Pennsylvania , 231 South 34th Street ,
      Philadelphia , Pennsylvania 19104 , United States.
FAU - Petersson, E James
AU  - Petersson EJ
AUID- ORCID: http://orcid.org/0000-0003-3854-9210
AD  - Department of Chemistry , University of Pennsylvania , 231 South 34th Street ,
      Philadelphia , Pennsylvania 19104 , United States.
LA  - eng
PT  - Journal Article
DEP - 20190123
PL  - United States
TA  - Biochemistry
JT  - Biochemistry
JID - 0370623
EDAT- 2019/02/20 06:00
MHDA- 2019/02/20 06:00
CRDT- 2019/02/20 06:00
PHST- 2019/02/20 06:00 [entrez]
PHST- 2019/02/20 06:00 [pubmed]
PHST- 2019/02/20 06:00 [medline]
AID - 10.1021/acs.biochem.8b01311 [doi]
PST - ppublish
SO  - Biochemistry. 2019 Feb 19;58(7):859-860. doi: 10.1021/acs.biochem.8b01311. Epub
      2019 Jan 23.

PMID- 30772369
OWN - NLM
STAT- In-Data-Review
LR  - 20190312
IS  - 1090-2430 (Electronic)
IS  - 0014-4886 (Linking)
VI  - 315
DP  - 2019 May
TI  - Parkinson's disease and pain: Modulation of nociceptive circuitry in a rat model 
      of nigrostriatal lesion.
PG  - 72-81
LID - S0014-4886(18)30509-0 [pii]
LID - 10.1016/j.expneurol.2019.02.007 [doi]
AB  - Parkinson's disease (PD) is a neurodegenerative disorder that causes progressive 
      dysfunction of dopaminergic and non-dopaminergic neurons, generating motor and
      nonmotor signs and symptoms. Pain is reported as the most bothersome nonmotor
      symptom in PD; however, pain remains overlooked and poorly understood. In this
      study, we evaluated the nociceptive behavior and the descending analgesia
      circuitry in a rat model of PD. Three independent experiments were performed to
      investigate: i) thermal nociceptive behavior; ii) mechanical nociceptive behavior
      and dopaminergic repositioning; and iii) modulation of the pain control
      circuitry. The rat model of PD, induced by unilateral striatal 6-hydroxydopamine 
      (6-OHDA), did not interfere with thermal nociceptive responses; however, the
      mechanical nociceptive threshold was decreased bilaterally compared to that of
      naive or striatal saline-injected rats. This response was reversed by apomorphine
      or levodopa treatment. Striatal 6-OHDA induced motor impairments and reduced
      dopaminergic neuron immunolabeling as well as the pattern of neuronal activation 
      (c-Fos) in the substantia nigra ipsilateral (IPL) to the lesion. In the midbrain 
      periaqueductal gray (PAG), 6-OHDA-induced lesion increased IPL and decreased
      contralateral PAG GABAergic labeling compared to control. In the dorsal horn of
      the spinal cord, lesioned rats showed bilateral inhibition of enkephalin and
      mu-opioid receptor labeling. Taken together, we demonstrated that the unilateral 
      6-OHDA-induced PD model induces bilateral mechanical hypernociception, which is
      reversed by dopamine restoration, changes in the PAG circuitry, and inhibition of
      spinal opioidergic regulation, probably due to impaired descending analgesic
      control. A better understanding of pain mechanisms in PD patients is critical for
      developing better therapeutic strategies to improve their quality of life.
CI  - Copyright (c) 2019 Elsevier Inc. All rights reserved.
FAU - Domenici, Roberta A
AU  - Domenici RA
AD  - Laboratory of Neuroscience, Hospital Sirio-Libanes, Sao Paulo, SP, Brazil.
FAU - Campos, Ana Carolina P
AU  - Campos ACP
AD  - Laboratory of Neuroscience, Hospital Sirio-Libanes, Sao Paulo, SP, Brazil.
FAU - Maciel, Soraya T
AU  - Maciel ST
AD  - Laboratory of Neuroscience, Hospital Sirio-Libanes, Sao Paulo, SP, Brazil.
FAU - Berzuino, Miria B
AU  - Berzuino MB
AD  - Laboratory of Neuroscience, Hospital Sirio-Libanes, Sao Paulo, SP, Brazil.
FAU - Hernandes, Marina S
AU  - Hernandes MS
AD  - Department of Medicine, Emory University, Atlanta, GA, United States of America.
FAU - Fonoff, Erich T
AU  - Fonoff ET
AD  - Laboratory of Neuroscience, Hospital Sirio-Libanes, Sao Paulo, SP, Brazil;
      Division of Functional Neurosurgery, Department of Neurology, University of Sao
      Paulo School of Medicine, Sao Paulo, SP, Brazil.
FAU - Pagano, Rosana L
AU  - Pagano RL
AD  - Laboratory of Neuroscience, Hospital Sirio-Libanes, Sao Paulo, SP, Brazil.
      Electronic address: rosana.lpagano@hsl.org.br.
LA  - eng
PT  - Journal Article
DEP - 20190214
PL  - United States
TA  - Exp Neurol
JT  - Experimental neurology
JID - 0370712
OTO - NOTNLM
OT  - Dopaminergic agonists
OT  - Enkephalin
OT  - GABA
OT  - Pain
OT  - Parkinson's disease
OT  - Periaqueductal gray
OT  - Spinal cord
EDAT- 2019/02/18 06:00
MHDA- 2019/02/18 06:00
CRDT- 2019/02/18 06:00
PHST- 2018/09/21 00:00 [received]
PHST- 2019/01/04 00:00 [revised]
PHST- 2019/02/11 00:00 [accepted]
PHST- 2019/02/18 06:00 [pubmed]
PHST- 2019/02/18 06:00 [medline]
PHST- 2019/02/18 06:00 [entrez]
AID - S0014-4886(18)30509-0 [pii]
AID - 10.1016/j.expneurol.2019.02.007 [doi]
PST - ppublish
SO  - Exp Neurol. 2019 May;315:72-81. doi: 10.1016/j.expneurol.2019.02.007. Epub 2019
      Feb 14.

PMID- 30794329
OWN - NLM
STAT- Publisher
LR  - 20190222
IS  - 1552-4604 (Electronic)
IS  - 0091-2700 (Linking)
DP  - 2019 Feb 22
TI  - Pharmacogenetic Profile and the Occurrence of Visual Hallucinations in Patients
      With Sporadic Parkinson's Disease.
LID - 10.1002/jcph.1394 [doi]
AB  - Visual hallucinations are significant nonmotor symptoms in the course of
      treatment of Parkinson's disease. Previous studies have shown that the
      interindividual variability and pharmacogenetic profile of Parkinson's disease
      patients seem to influence the occurrence of visual hallucinations. In our study,
      we investigated a possible relationship of sequence variants in DRD1, DRD2, DRD3,
      DAT1, and COMT genes with the presence of visual hallucinations in Parkinson's
      disease patients. A total of 224 Brazilian patients from the Pro-Parkinson
      service at the Clinical Hospital of the University of Pernambuco, diagnosed with 
      sporadic Parkinson's disease, were enrolled. Parkinson's disease patients were
      divided into 2 groups based on the presence or absence of visual hallucinations. 
      The sequence variants for DRD1, DRD2, DRD3, DAT1, and COMT were determined
      through the polymerase chain reaction-restriction fragment length polymorphism
      technique. Multiple Poisson regression analyses showed that individuals carrying 
      the DRD3 Ser/Ser and Ser/Gly genotypes presented increased prevalence ratios of
      visual hallucinations (9.7-fold and 4.4-fold, respectively; P < .001). Regarding 
      DAT1 rs28363170, there was a 9.82-fold increase in the prevalence ratio in
      patients with the 10/11 genotype, 8.78-fold for the 10/8 genotype, and 2.44-fold 
      for the 9/8 genotypes (P < .001, for all). In addition, visual hallucinations
      were also associated with use of transdermal patches with rotigotine (PR, 3.7;
      95%CI, 1.2-10.9; P = .017) and rasagiline (PR, 2.8; 95%CI, 1.3-6.0; P = .006).
      Our results suggest that the genetic variants DRD3 and DAT1, along with other
      therapeutic confounders, may influence the prevalence ratio of visual
      hallucinations.
CI  - (c) 2019, The American College of Clinical Pharmacology.
FAU - Damasceno Dos Santos, Erinaldo Ubirajara
AU  - Damasceno Dos Santos EU
AUID- ORCID: https://orcid.org/0000-0003-2077-4794
AD  - Graduate Program in Applied Cellular and Molecular Biology, University of
      Pernambuco (UPE), Recife, PE, Brazil.
FAU - Duarte, Elaine Bandeira Cavalcanti
AU  - Duarte EBC
AD  - Graduate Program in Applied Biology for Health, Federal University of Pernambuco 
      (UFPE), Recife, PE, Brazil.
FAU - Miranda, Laura Maria Ramos
AU  - Miranda LMR
AD  - Department of Biology, Federal Rural University of Pernambuco (UFRPE), Recife,
      PE, Brazil.
FAU - Asano, Amdore Guescel C
AU  - Asano AGC
AD  - Department of Clinical Medicine, Faculty of Medicine, Federal University of
      Pernambuco (UFPE), Recife, PE, Brazil.
AD  - Pro-Parkinson Program of the Clinical Hospital of the Federal University of
      Pernambuco Recife (HC/UFPE), Recife, PE, Brazil.
FAU - Asano, Nadja Maria Jorge
AU  - Asano NMJ
AD  - Department of Clinical Medicine, Faculty of Medicine, Federal University of
      Pernambuco (UFPE), Recife, PE, Brazil.
AD  - Pro-Parkinson Program of the Clinical Hospital of the Federal University of
      Pernambuco Recife (HC/UFPE), Recife, PE, Brazil.
FAU - Maia, Maria De Mascena Diniz
AU  - Maia MMD
AD  - Department of Biology, Federal Rural University of Pernambuco (UFRPE), Recife,
      PE, Brazil.
FAU - de Souza, Paulo Roberto Eleuterio
AU  - de Souza PRE
AUID- ORCID: https://orcid.org/0000-0002-9186-9849
AD  - Graduate Program in Applied Cellular and Molecular Biology, University of
      Pernambuco (UPE), Recife, PE, Brazil.
AD  - Graduate Program in Applied Biology for Health, Federal University of Pernambuco 
      (UFPE), Recife, PE, Brazil.
AD  - Department of Biology, Federal Rural University of Pernambuco (UFRPE), Recife,
      PE, Brazil.
LA  - eng
GR  - FACEPE
GR  - CAPES
PT  - Journal Article
DEP - 20190222
PL  - England
TA  - J Clin Pharmacol
JT  - Journal of clinical pharmacology
JID - 0366372
OTO - NOTNLM
OT  - DAT1
OT  - DRD3
OT  - Parkinson's disease
OT  - pharmacogenetics
OT  - visual hallucinations
EDAT- 2019/02/23 06:00
MHDA- 2019/02/23 06:00
CRDT- 2019/02/23 06:00
PHST- 2018/10/03 00:00 [received]
PHST- 2019/01/30 00:00 [accepted]
PHST- 2019/02/23 06:00 [entrez]
PHST- 2019/02/23 06:00 [pubmed]
PHST- 2019/02/23 06:00 [medline]
AID - 10.1002/jcph.1394 [doi]
PST - aheadofprint
SO  - J Clin Pharmacol. 2019 Feb 22. doi: 10.1002/jcph.1394.

PMID- 30782975
OWN - NLM
STAT- Publisher
LR  - 20190220
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Linking)
DP  - 2019 Feb 19
TI  - Optogenetic stimulation of the M2 cortex reverts motor dysfunction in a mouse
      model of Parkinson's Disease.
LID - 2277-18 [pii]
LID - 10.1523/JNEUROSCI.2277-18.2019 [doi]
AB  - Neuromodulation of deep brain structures (deep brain stimulation - DBS) is the
      current surgical procedure for treatment of Parkinson's disease. Less studied is 
      the stimulation of cortical motor areas to treat PD symptoms, although also known
      to alleviate motor disturbances in PD. We were able to show that optogenetic
      activation of secondary (M2) motor cortex improves motor functions in
      dopamine-depleted male mice. The stimulated M2 cortex harbors glutamatergic
      pyramidal neurons that project to subcortical structures, critically involved in 
      motor control, and makes synaptic contacts with dopaminergic neurons. Strikingly,
      optogenetic activation of M2 neurons or axons into the dorsomedial striatum
      increases striatal levels of dopamine and evokes locomotor activity. We found
      that dopamine neurotransmission sensitizes the locomotor behavior elicited by
      activation of M2 neurons. Furthermore, combination of intranigral infusion of
      glutamatergic antagonists and circuit specific optogenetic stimulation revealed
      that behavioral response depended on the activity of M2 neurons projecting to
      substantia nigra pars compacta (SNc). Interestingly, repeated M2 stimulation
      combined with L-DOPA treatment produced an unanticipated improvement in working
      memory performance, which was absent in control mice under L-DOPA treatment only.
      Therefore, the M2-basal ganglia circuit is critical for the assembly of the motor
      and cognitive function, and this study demonstrates a therapeutic mechanism for
      cortical stimulation in PD that involves recruitment of long-range glutamatergic 
      projection neurons.SIGNIFICANCE STATEMENTSome patients with Parkinson's disease
      are offered treatment through surgery, which consists of delivering electrical
      current to regions deep within the brain. This study shows that stimulation of an
      area located on the brain surface, known as the secondary motor cortex, can also 
      reverse movement disorders in mice. Authors have used a brain stimulation
      technique called optogenetics, which allowed targeting a specific type of surface
      neuron that communicates with the deep part of the brain involved in movement
      control. The study also shows that a combination of this stimulation with drug
      treatment might be useful to treat memory impairment, a kind of cognitive problem
      in Parkinson's.
CI  - Copyright (c) 2019 the authors.
FAU - Viana Magno, Luiz Alexandre
AU  - Viana Magno LA
AD  - Centro de Tecnologia em Medicina Molecular.
FAU - Tenza-Ferrer, Helia
AU  - Tenza-Ferrer H
AD  - Centro de Tecnologia em Medicina Molecular.
FAU - Collodetti, Melcar
AU  - Collodetti M
AD  - Centro de Tecnologia em Medicina Molecular.
FAU - Felipe Guimaraes Aguiar, Matheus
AU  - Felipe Guimaraes Aguiar M
AD  - Centro de Tecnologia em Medicina Molecular.
FAU - Paula Carneiro Rodrigues, Ana
AU  - Paula Carneiro Rodrigues A
AD  - Centro de Tecnologia em Medicina Molecular.
FAU - Souza da Silva, Rodrigo
AU  - Souza da Silva R
AD  - Centro de Tecnologia em Medicina Molecular.
FAU - do Prado Silva, Joice
AU  - do Prado Silva J
AD  - Centro de Tecnologia em Medicina Molecular.
FAU - Ferreira Nicolau, Nycolle
AU  - Ferreira Nicolau N
AD  - Centro de Tecnologia em Medicina Molecular.
FAU - Valadao Freitas Rosa, Daniela
AU  - Valadao Freitas Rosa D
AD  - Centro de Tecnologia em Medicina Molecular.
FAU - Birbrair, Alexander
AU  - Birbrair A
AD  - Departamento de Patologia, Instituto de Ciencias Biologicas, Universidade Federal
      de Minas Gerais (UFMG), Belo Horizonte, Brazil.
FAU - Marques Miranda, Debora
AU  - Marques Miranda D
AD  - Centro de Tecnologia em Medicina Molecular.
AD  - Departamento de Pediatria, Faculdade de Medicina, Universidade Federal de Minas
      Gerais (UFMG), Belo Horizonte, Brazil.
FAU - Aurelio Romano-Silva, Marco
AU  - Aurelio Romano-Silva M
AD  - Centro de Tecnologia em Medicina Molecular romano-silva@ufmg.br.
AD  - Departamento de Saude Mental e.
LA  - eng
PT  - Journal Article
DEP - 20190219
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for
      Neuroscience
JID - 8102140
EDAT- 2019/02/21 06:00
MHDA- 2019/02/21 06:00
CRDT- 2019/02/21 06:00
PHST- 2018/09/03 00:00 [received]
PHST- 2019/02/01 00:00 [revised]
PHST- 2019/02/04 00:00 [accepted]
PHST- 2019/02/21 06:00 [entrez]
PHST- 2019/02/21 06:00 [pubmed]
PHST- 2019/02/21 06:00 [medline]
AID - JNEUROSCI.2277-18.2019 [pii]
AID - 10.1523/JNEUROSCI.2277-18.2019 [doi]
PST - aheadofprint
SO  - J Neurosci. 2019 Feb 19. pii: JNEUROSCI.2277-18.2019. doi:
      10.1523/JNEUROSCI.2277-18.2019.

PMID- 30776152
OWN - NLM
STAT- In-Data-Review
LR  - 20190416
IS  - 1531-8257 (Electronic)
IS  - 0885-3185 (Linking)
VI  - 34
IP  - 2
DP  - 2019 Feb
TI  - Comparative sensitivity of the MoCA and Mattis Dementia Rating Scale-2 in
      Parkinson's disease.
PG  - 285-291
LID - 10.1002/mds.27575 [doi]
AB  - BACKGROUND: Clinicians and researchers commonly use global cognitive assessments 
      to screen for impairment. Currently there are no published studies directly
      comparing the sensitivity and specificity of the Montreal Cognitive Assessment
      and Mattis Dementia Rating Scale-2 in PD. The objective of this study was to
      identify the relative sensitivity and specificity of the Montreal Cognitive
      Assessment and Mattis Dementia Rating Scale-2 in PD. METHODS: The Montreal
      Cognitive Assessment and Mattis Dementia Rating Scale-2 were administered to
      training and validation cohorts. Cutoff scores were determined within the
      training cohort (n = 85) to optimize sensitivity and specificity for cognitive
      impairment and were applied to an independent validation cohort (n = 521).
      RESULTS: The Montreal Cognitive Assessment was consistently sensitive across
      training and validation cohorts (90.0% and 80.3%, respectively), whereas the
      Mattis Dementia Rating Scale-2 was not (87.5% and 60.3%, respectively). In
      individual domains, the Montreal Cognitive Assessment remained sensitive to
      memory and visuospatial impairments (91.9% and 87.8%, respectively), whereas the 
      Mattis Dementia Rating Scale-2 was sensitive to executive impairments (86.2%).
      CONCLUSION: The Montreal Cognitive Assessment and Mattis Dementia Rating Scale-2 
      demonstrated individual strengths. Future work should focus on developing
      domain-specific cognitive screening tools for PD. (c) 2018 International
      Parkinson and Movement Disorder Society.
CI  - (c) 2018 International Parkinson and Movement Disorder Society.
FAU - Hendershott, Taylor R
AU  - Hendershott TR
AD  - Department of Psychological and Brain Sciences, Washington University, St. Louis,
      Missouri, USA.
FAU - Zhu, Delphine
AU  - Zhu D
AD  - Department of Neurology and Neurological Sciences, Stanford University School of 
      Medicine, Stanford, California, USA.
FAU - Llanes, Seoni
AU  - Llanes S
AD  - Department of Neurology and Neurological Sciences, Stanford University School of 
      Medicine, Stanford, California, USA.
FAU - Zabetian, Cyrus P
AU  - Zabetian CP
AD  - Veterans Affairs Puget Sound Health Care System, Seattle, Washington, USA.
AD  - Department of Neurology, University of Washington School of Medicine, Seattle,
      Washington, USA.
FAU - Quinn, Joseph
AU  - Quinn J
AD  - Department of Neurology, Oregon Health Sciences University, Portland, Oregon,
      USA.
FAU - Edwards, Karen L
AU  - Edwards KL
AD  - Department of Epidemiology, University of California, Irvine School of Medicine, 
      Irvine, California, USA.
FAU - Leverenz, James B
AU  - Leverenz JB
AD  - Lou Ruvo Center for Brain Health, Neurological Institute, Cleveland Clinic,
      Cleveland, Ohio, USA.
FAU - Montine, Thomas
AU  - Montine T
AD  - Department of Pathology, Stanford University School of Medicine, Stanford,
      California, USA.
FAU - Cholerton, Brenna
AU  - Cholerton B
AD  - Department of Neurology and Neurological Sciences, Stanford University School of 
      Medicine, Stanford, California, USA.
FAU - Poston, Kathleen L
AU  - Poston KL
AD  - Department of Neurology and Neurological Sciences, Stanford University School of 
      Medicine, Stanford, California, USA.
AD  - Department of Neurosurgery, Stanford University School of Medicine, Stanford,
      California, USA.
LA  - eng
GR  - P50 NS071675/National Institute of Neurological Disorder and Stroke
GR  - Michael J. Fox Foundation for Parkinson's Research
GR  - U01 NS100610/NS/NINDS NIH HHS/United States
GR  - P50 NS071675/NS/NINDS NIH HHS/United States
GR  - P50 NS062684/NS/NINDS NIH HHS/United States
GR  - K23 NS075097/NS/NINDS NIH HHS/United States
GR  - K23 NS075097/National Institute of Neurological Disorder and Stroke
GR  - P50 AG047366/AG/NIA NIH HHS/United States
GR  - P50 NS062684/National Institute of Neurological Disorder and Stroke
GR  - P50 AG047366/National Institute on Aging
GR  - DGE-1745038/National Science Foundation
GR  - UO1 NS100610/National Institute of Neurological Disorder and Stroke
PT  - Journal Article
DEP - 20181210
PL  - United States
TA  - Mov Disord
JT  - Movement disorders : official journal of the Movement Disorder Society
JID - 8610688
OTO - NOTNLM
OT  - Mattis Dementia Rating Scale-2
OT  - Montreal Cognitive Assessment
OT  - Parkinson's disease
OT  - cognitive impairment
EDAT- 2019/02/19 06:00
MHDA- 2019/02/19 06:00
CRDT- 2019/02/19 06:00
PHST- 2018/08/14 00:00 [received]
PHST- 2018/10/24 00:00 [revised]
PHST- 2018/10/26 00:00 [accepted]
PHST- 2019/02/19 06:00 [entrez]
PHST- 2019/02/19 06:00 [pubmed]
PHST- 2019/02/19 06:00 [medline]
AID - 10.1002/mds.27575 [doi]
PST - ppublish
SO  - Mov Disord. 2019 Feb;34(2):285-291. doi: 10.1002/mds.27575. Epub 2018 Dec 10.

PMID- 30788890
OWN - NLM
STAT- In-Data-Review
LR  - 20190419
IS  - 1531-8257 (Electronic)
IS  - 0885-3185 (Linking)
VI  - 34
IP  - 4
DP  - 2019 Apr
TI  - SMPD1 mutations, activity, and alpha-synuclein accumulation in Parkinson's
      disease.
PG  - 526-535
LID - 10.1002/mds.27642 [doi]
AB  - BACKGROUND: SMPD1 (acid-sphingomyelinase) variants have been associated with
      Parkinson's disease in recent studies. The objective of this study was to further
      investigate the role of SMPD1 mutations in PD. METHODS: SMPD1 was sequenced in 3 
      cohorts (Israel Ashkenazi Jewish cohort, Montreal/Montpellier, and New York),
      including 1592 PD patients and 975 controls. Additional data were available for
      10,709 Ashkenazi Jewish controls. Acid-sphingomyelinase activity was measured by 
      a mass spectrometry-based assay in the New York cohort. alpha-Synuclein levels
      were measured in vitro following CRISPR/Cas9-mediated knockout and siRNA
      knockdown of SMPD1 in HeLa and BE(2)-M17 cells. Lysosomal localization of
      acid-sphingomyelinase with different mutations was studied, and in silico
      analysis of their effect on acid-sphingomyelinase structure was performed.
      RESULTS: SMPD1 mutations were associated with PD in the Ashkenazi Jewish cohort, 
      as 1.4% of PD patients carried the p.L302P or p.fsP330 mutation, compared with
      0.37% in 10,709 Ashkenazi Jewish controls (OR, 3.7; 95%CI, 1.6-8.2; P = 0.0025). 
      In the Montreal/Montpellier cohort, the p.A487V variant was nominally associated 
      with PD (1.5% versus 0.14%; P = 0.0065, not significant after correction for
      multiple comparisons). Among PD patients, reduced acid-sphingomyelinase activity 
      was associated with a 3.5- to 5.8-year earlier onset of PD in the lowest quartile
      versus the highest quartile of acid-sphingomyelinase activity (P = 0.01-0.001).
      We further demonstrated that SMPD1 knockout and knockdown resulted in increased
      alpha-synuclein levels in HeLa and BE(2)-M17 dopaminergic cells and that the
      p.L302P and p.fsP330 mutations impair the traffic of acid-sphingomyelinase to the
      lysosome. CONCLUSIONS: Our results support an association between SMPD1 variants,
      acid-sphingomyelinase activity, and PD. Furthermore, they suggest that reduced
      acid-sphingomyelinase activity may lead to alpha-synuclein accumulation. (c) 2019
      International Parkinson and Movement Disorder Society.
CI  - (c) 2019 International Parkinson and Movement Disorder Society.
FAU - Alcalay, Roy N
AU  - Alcalay RN
AD  - Department of Neurology, College of Physicians and Surgeons, Columbia University,
      New York, NY, USA.
AD  - Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia 
      University, New York, NY, USA.
FAU - Mallett, Victoria
AU  - Mallett V
AD  - Montreal Neurological Institute, McGill University, Montreal, QC, Canada.
FAU - Vanderperre, Benoit
AU  - Vanderperre B
AD  - McGill Parkinson Program and Neurodegenerative Diseases Group, Montreal
      Neurological Institute, McGill University, Montreal, QC, Canada.
FAU - Tavassoly, Omid
AU  - Tavassoly O
AD  - McGill Parkinson Program and Neurodegenerative Diseases Group, Montreal
      Neurological Institute, McGill University, Montreal, QC, Canada.
FAU - Dauvilliers, Yves
AU  - Dauvilliers Y
AD  - Sleep Unit, National Reference Network for Narcolepsy, Department of Neurology
      Hopital-Gui-de Chauliac, CHU Montpellier, INSERM U1061, France.
FAU - Wu, Richard Y J
AU  - Wu RYJ
AD  - Montreal Neurological Institute, McGill University, Montreal, QC, Canada.
AD  - Imperial College School of Medicine, Imperial College London, London, United
      Kingdom.
FAU - Ruskey, Jennifer A
AU  - Ruskey JA
AD  - Montreal Neurological Institute, McGill University, Montreal, QC, Canada.
AD  - Department of Neurology and Neurosurgery, McGill University, Montreal, QC,
      Canada.
FAU - Leblond, Claire S
AU  - Leblond CS
AD  - Montreal Neurological Institute, McGill University, Montreal, QC, Canada.
AD  - Department of Human Genetics, McGill University, Montreal, QC, Canada.
FAU - Ambalavanan, Amirthagowri
AU  - Ambalavanan A
AD  - Montreal Neurological Institute, McGill University, Montreal, QC, Canada.
AD  - Department of Human Genetics, McGill University, Montreal, QC, Canada.
FAU - Laurent, Sandra B
AU  - Laurent SB
AD  - Montreal Neurological Institute, McGill University, Montreal, QC, Canada.
AD  - Department of Neurology and Neurosurgery, McGill University, Montreal, QC,
      Canada.
FAU - Spiegelman, Dan
AU  - Spiegelman D
AD  - Montreal Neurological Institute, McGill University, Montreal, QC, Canada.
AD  - Department of Neurology and Neurosurgery, McGill University, Montreal, QC,
      Canada.
FAU - Dionne-Laporte, Alexandre
AU  - Dionne-Laporte A
AD  - Montreal Neurological Institute, McGill University, Montreal, QC, Canada.
AD  - Department of Neurology and Neurosurgery, McGill University, Montreal, QC,
      Canada.
FAU - Liong, Christopher
AU  - Liong C
AD  - Department of Neurology, College of Physicians and Surgeons, Columbia University,
      New York, NY, USA.
FAU - Levy, Oren A
AU  - Levy OA
AD  - Department of Neurology, College of Physicians and Surgeons, Columbia University,
      New York, NY, USA.
FAU - Fahn, Stanley
AU  - Fahn S
AD  - Department of Neurology, College of Physicians and Surgeons, Columbia University,
      New York, NY, USA.
FAU - Waters, Cheryl
AU  - Waters C
AD  - Department of Neurology, College of Physicians and Surgeons, Columbia University,
      New York, NY, USA.
FAU - Kuo, Sheng-Han
AU  - Kuo SH
AD  - Department of Neurology, College of Physicians and Surgeons, Columbia University,
      New York, NY, USA.
FAU - Chung, Wendy K
AU  - Chung WK
AD  - Department of Medicine, College of Physicians and Surgeons, Columbia University, 
      New York, NY, USA.
AD  - Department of Pediatrics, College of Physicians and Surgeons, Columbia
      University, New York, NY, USA.
FAU - Ford, Blair
AU  - Ford B
AD  - Department of Neurology, College of Physicians and Surgeons, Columbia University,
      New York, NY, USA.
FAU - Marder, Karen S
AU  - Marder KS
AD  - Department of Neurology, College of Physicians and Surgeons, Columbia University,
      New York, NY, USA.
FAU - Kang, Un Jung
AU  - Kang UJ
AD  - Department of Neurology, College of Physicians and Surgeons, Columbia University,
      New York, NY, USA.
FAU - Hassin-Baer, Sharon
AU  - Hassin-Baer S
AD  - Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
AD  - Department of Neurology, Sheba Medical Center, Tel Hashomer, Israel.
AD  - Movement Disorders Institute, Sheba Medical Center, Tel Hashomerf, Israel.
FAU - Greenbaum, Lior
AU  - Greenbaum L
AD  - Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
AD  - The Danek Gertner Institute of Human Genetics, Sheba Medical Center, Tel
      Hashomer, Israel.
AD  - The Joseph Sagol Neuroscience Center, Sheba Medical Center, Tel Hashomer, Israel.
FAU - Trempe, Jean-Francois
AU  - Trempe JF
AD  - Department of Pharmacology & Therapeutics, McGill University, Montreal, Quebec,
      Canada.
FAU - Wolf, Pavlina
AU  - Wolf P
AD  - Translational Science, Sanofi, Framingham, MA, USA.
FAU - Oliva, Petra
AU  - Oliva P
AD  - Translational Science, Sanofi, Framingham, MA, USA.
FAU - Zhang, Xiaokui Kate
AU  - Zhang XK
AD  - Translational Science, Sanofi, Framingham, MA, USA.
FAU - Clark, Lorraine N
AU  - Clark LN
AD  - Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia 
      University, New York, NY, USA.
AD  - Laboratory of Personalized Genomic Medicine, Department of Pathology and Cell
      Biology, Columbia University, New York, NY, USA.
AD  - Department of Pathology and Cell Biology, Columbia University, New York, NY, USA.
FAU - Langlois, Melanie
AU  - Langlois M
AD  - Axe neurosciences du CHU de Quebec - Universite Laval, Quebec, QC, Canada.
AD  - Faculty of Medicine, Department of Medicine, Laval University, Quebec, QC,
      Canada.
FAU - Dion, Patrick A
AU  - Dion PA
AD  - Montreal Neurological Institute, McGill University, Montreal, QC, Canada.
AD  - Department of Neurology and Neurosurgery, McGill University, Montreal, QC,
      Canada.
FAU - Fon, Edward A
AU  - Fon EA
AD  - McGill Parkinson Program and Neurodegenerative Diseases Group, Montreal
      Neurological Institute, McGill University, Montreal, QC, Canada.
FAU - Dupre, Nicolas
AU  - Dupre N
AD  - Axe neurosciences du CHU de Quebec - Universite Laval, Quebec, QC, Canada.
AD  - Faculty of Medicine, Department of Medicine, Laval University, Quebec, QC,
      Canada.
FAU - Rouleau, Guy A
AU  - Rouleau GA
AD  - Montreal Neurological Institute, McGill University, Montreal, QC, Canada.
AD  - Department of Neurology and Neurosurgery, McGill University, Montreal, QC,
      Canada.
AD  - Department of Human Genetics, McGill University, Montreal, QC, Canada.
FAU - Gan-Or, Ziv
AU  - Gan-Or Z
AUID- ORCID: https://orcid.org/0000-0003-0332-234X
AD  - Montreal Neurological Institute, McGill University, Montreal, QC, Canada.
AD  - Department of Neurology and Neurosurgery, McGill University, Montreal, QC,
      Canada.
AD  - Department of Human Genetics, McGill University, Montreal, QC, Canada.
LA  - eng
GR  - K02NS080915/National Institutes of Health
GR  - Michael J. Fox Foundation for Parkinson's Research
GR  - K02 NS080915/NS/NINDS NIH HHS/United States
GR  - U10 NS077267/NS/NINDS NIH HHS/United States
GR  - UL1 TR000040/National Institutes of Health
GR  - R01 NS101982/NS/NINDS NIH HHS/United States
GR  - Brookdale Foundation
GR  - Parkinson's Disease Foundation
GR  - R03 NS096494/NS/NINDS NIH HHS/United States
GR  - Canadian Consortium om Neurodegeneration in Aging (CCNA)
GR  - Fonds de Recherche du Quebec - Sante
GR  - UL1 TR000040/TR/NCATS NIH HHS/United States
GR  - R56 NS036630/NS/NINDS NIH HHS/United States
GR  - Canadian Institutes of Health Research
GR  - R01 NS036630/NS/NINDS NIH HHS/United States
PT  - Journal Article
DEP - 20190220
PL  - United States
TA  - Mov Disord
JT  - Movement disorders : official journal of the Movement Disorder Society
JID - 8610688
PMC - PMC6469643
MID - NIHMS1017870
OTO - NOTNLM
OT  - SMPD1
OT  - Parkinson's disease
OT  - acid sphingomyelinase
OT  - genetics
OT  - alpha-synuclein
EDAT- 2019/02/23 06:00
MHDA- 2019/02/23 06:00
CRDT- 2019/02/22 06:00
PMCR- 2020/04/01 00:00
PHST- 2018/02/14 00:00 [received]
PHST- 2018/11/21 00:00 [revised]
PHST- 2019/01/10 00:00 [accepted]
PHST- 2020/04/01 00:00 [pmc-release]
PHST- 2019/02/23 06:00 [pubmed]
PHST- 2019/02/23 06:00 [medline]
PHST- 2019/02/22 06:00 [entrez]
AID - 10.1002/mds.27642 [doi]
PST - ppublish
SO  - Mov Disord. 2019 Apr;34(4):526-535. doi: 10.1002/mds.27642. Epub 2019 Feb 20.

PMID- 30788857
OWN - NLM
STAT- In-Data-Review
LR  - 20190416
IS  - 1531-8257 (Electronic)
IS  - 0885-3185 (Linking)
VI  - 34
IP  - 4
DP  - 2019 Apr
TI  - A clinical and genetic study of early-onset and familial parkinsonism in taiwan: 
      An integrated approach combining gene dosage analysis and next-generation
      sequencing.
PG  - 506-515
LID - 10.1002/mds.27633 [doi]
AB  - BACKGROUND: Recent genetic progress has allowed for the molecular diagnosis of
      Parkinson's disease. However, genetic causes of PD vary widely in different
      ethnicities. Mutational frequencies and clinical phenotypes of genes associated
      with PD in Asian populations are largely unknown. The objective of this study was
      to identify the mutational frequencies and clinical spectrums of multiple
      PD-causative genes in a Taiwanese PD cohort. METHODS: A total of 571 participants
      including 324 patients with early-onset parkinsonism (onset age, <50 years) and
      247 parkinsonism pedigrees were recruited at a tertiary referral center in Taiwan
      from 2002 to 2017. Genetic causes were identified by an integrated approach
      including gene dosage analysis, a targeted next-generation sequencing panel
      containing 40 known PD-causative genes, repeat-primed polymerase chain reaction, 
      and whole-exome sequencing analysis. RESULTS: Thirty of the 324 patients with
      early-onset parkinsonism (9.3%) were found to carry mutations in Parkin, PINK1,
      or PLA2G6 or had increased trinucleotide repeats in SCA8. Twenty-nine of 109
      probands with autosomal-recessive inheritance of parkinsonism (26.6%) were found 
      to carry mutations in Parkin, PINK1, GBA, or HTRA2. The genetic causes for the
      138 probands with an autosomal-dominant inheritance pattern of parkinsonism were 
      more heterogeneous. Seventeen probands (12.3%) carried pathogenic mutations in
      LRRK2, VPS35, MAPT, GBA, DNAJC13, C9orf72, SCA3, or SCA17. A novel missense
      mutation in the UQCRC1 gene was found in a family with autosomal-dominant
      inheritance parkinsonism via whole-exome sequencing analysis. CONCLUSIONS: Our
      findings provide a better understanding of the genetic architecture of PD in
      eastern Asia and broaden the clinical spectrum of PD-causing mutations. (c) 2019 
      The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of
      International Parkinson and Movement Disorder Society.
CI  - (c) 2019 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on 
      behalf of International Parkinson and Movement Disorder Society.
FAU - Lin, Chin-Hsien
AU  - Lin CH
AUID- ORCID: https://orcid.org/0000-0001-8566-7573
AD  - Department of Neurology, Centre of Parkinson and Movement Disorders, National
      Taiwan University Hospital, College of Medicine, National Taiwan University,
      Taipei, Taiwan.
FAU - Chen, Pei-Lung
AU  - Chen PL
AD  - Department of Medical Genetics, National Taiwan University Hospital, Taipei,
      Taiwan.
AD  - Graduate Institute of Medical Genomics and Proteomics, National Taiwan University
      College of Medicine, Taipei, Taiwan.
FAU - Tai, Chun-Hwei
AU  - Tai CH
AD  - Department of Neurology, Centre of Parkinson and Movement Disorders, National
      Taiwan University Hospital, College of Medicine, National Taiwan University,
      Taipei, Taiwan.
FAU - Lin, Hang-I
AU  - Lin HI
AD  - Department of Neurology, Centre of Parkinson and Movement Disorders, National
      Taiwan University Hospital, College of Medicine, National Taiwan University,
      Taipei, Taiwan.
FAU - Chen, Chih-Shan
AU  - Chen CS
AD  - Department of Medical Genetics, National Taiwan University Hospital, Taipei,
      Taiwan.
FAU - Chen, Meng-Ling
AU  - Chen ML
AD  - Department of Neurology, Centre of Parkinson and Movement Disorders, National
      Taiwan University Hospital, College of Medicine, National Taiwan University,
      Taipei, Taiwan.
FAU - Wu, Ruey-Meei
AU  - Wu RM
AD  - Department of Neurology, Centre of Parkinson and Movement Disorders, National
      Taiwan University Hospital, College of Medicine, National Taiwan University,
      Taipei, Taiwan.
LA  - eng
GR  - MOST 106-2314-B-002-072-MY3/Ministry of Science and Technology, Taiwan
GR  - 106R8805C1/National Taiwan University
GR  - NTUH 107C101-82/National Taiwan University Hospital
GR  - N.A./T.H. Wu Foundation
PT  - Journal Article
DEP - 20190220
PL  - United States
TA  - Mov Disord
JT  - Movement disorders : official journal of the Movement Disorder Society
JID - 8610688
OTO - NOTNLM
OT  - Parkinson's disease
OT  - early onset
OT  - genetics
OT  - next-generation sequencing
OT  - parkinsonism
EDAT- 2019/02/23 06:00
MHDA- 2019/02/23 06:00
CRDT- 2019/02/22 06:00
PHST- 2018/07/17 00:00 [received]
PHST- 2019/01/10 00:00 [revised]
PHST- 2019/01/14 00:00 [accepted]
PHST- 2019/02/23 06:00 [pubmed]
PHST- 2019/02/23 06:00 [medline]
PHST- 2019/02/22 06:00 [entrez]
AID - 10.1002/mds.27633 [doi]
PST - ppublish
SO  - Mov Disord. 2019 Apr;34(4):506-515. doi: 10.1002/mds.27633. Epub 2019 Feb 20.

PMID- 30773680
OWN - NLM
STAT- In-Data-Review
LR  - 20190416
IS  - 1531-8257 (Electronic)
IS  - 0885-3185 (Linking)
VI  - 34
IP  - 4
DP  - 2019 Apr
TI  - Clinical heterogeneity of frontotemporal dementia and Parkinsonism linked to
      chromosome 17 caused by MAPT N279K mutation in relation to tau positron emission 
      tomography features.
PG  - 568-574
LID - 10.1002/mds.27623 [doi]
AB  - BACKGROUND: While mechanistic links between tau abnormalities and
      neurodegeneration have been proven in frontotemporal dementia and parkinsonism
      linked to chromosome 17 caused by MAPT mutations, variability of the tau
      pathogenesis and its relation to clinical progressions in the same MAPT mutation 
      carriers are yet to be clarified. OBJECTIVES: The present study aimed to analyze 
      clinical profiles, tau accumulations, and their correlations in 3 kindreds with
      frontotemporal dementia and parkinsonism linked to chromosome 17 attributed to
      the MAPT N279K mutation. METHODS: Four patients with N279K mutant frontotemporal 
      dementia and parkinsonism linked to chromosome 17/MAPT underwent [(11) C]PBB3-PET
      to estimate regional tau loads. RESULTS: Haplotype assays revealed that these
      kindreds originated from a single founder. Despite homogeneity of the
      disease-causing MAPT allele, clinical progression was more rapid in 2 kindreds
      than in the other. The kindred with slow progression showed mild tau depositions,
      mostly confined to the midbrain and medial temporal areas. In contrast, kindreds 
      with rapid progression showed profoundly increased [(11) C]PBB3 binding in
      widespread regions from an early disease stage. CONCLUSIONS: [(11) C]PBB3-PET can
      capture four-repeat tau pathologies characteristic of N279K mutant frontotemporal
      dementia and parkinsonism linked to chromosome 17/MAPT. Our findings indicate
      that, in addition to the mutated MAPT allele, genetic and/or epigenetic modifiers
      of tau pathologies lead to heterogeneous clinicopathological features. (c) 2019
      The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of
      International Parkinson and Movement Disorder Society.
CI  - (c) 2019 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on 
      behalf of International Parkinson and Movement Disorder Society.
FAU - Ikeda, Aya
AU  - Ikeda A
AD  - Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
FAU - Shimada, Hitoshi
AU  - Shimada H
AD  - Department of Functional Brain Imaging Research, National Institute of
      Radiological Sciences, National Institutes for Quantum and Radiological Science
      and Technology, Chiba, Japan.
FAU - Nishioka, Kenya
AU  - Nishioka K
AD  - Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
FAU - Takanashi, Masashi
AU  - Takanashi M
AD  - Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
FAU - Hayashida, Arisa
AU  - Hayashida A
AD  - Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
FAU - Li, Yuanzhe
AU  - Li Y
AD  - Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
FAU - Yoshino, Hiroyo
AU  - Yoshino H
AD  - Research Institute for Diseases of Old Age, Graduate School of Medicine, Juntendo
      University, Tokyo, Japan.
FAU - Funayama, Manabu
AU  - Funayama M
AD  - Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
AD  - Research Institute for Diseases of Old Age, Graduate School of Medicine, Juntendo
      University, Tokyo, Japan.
FAU - Ueno, Yuji
AU  - Ueno Y
AD  - Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
FAU - Hatano, Taku
AU  - Hatano T
AD  - Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
FAU - Sahara, Naruhiko
AU  - Sahara N
AD  - Department of Functional Brain Imaging Research, National Institute of
      Radiological Sciences, National Institutes for Quantum and Radiological Science
      and Technology, Chiba, Japan.
FAU - Suhara, Tetsuya
AU  - Suhara T
AD  - Department of Functional Brain Imaging Research, National Institute of
      Radiological Sciences, National Institutes for Quantum and Radiological Science
      and Technology, Chiba, Japan.
FAU - Higuchi, Makoto
AU  - Higuchi M
AD  - Department of Functional Brain Imaging Research, National Institute of
      Radiological Sciences, National Institutes for Quantum and Radiological Science
      and Technology, Chiba, Japan.
FAU - Hattori, Nobutaka
AU  - Hattori N
AD  - Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
AD  - Research Institute for Diseases of Old Age, Graduate School of Medicine, Juntendo
      University, Tokyo, Japan.
LA  - eng
GR  - 15ek0109029s0202/Japan Agency for Medical Research and Development
GR  - 16768966/Japan Agency for Medical Research and Development
GR  - 16K09678/Ministry of Education, Culture, Sports, Science and Technology
GR  - 26713031/Ministry of Education, Culture, Sports, Science and Technology
PT  - Journal Article
DEP - 20190217
PL  - United States
TA  - Mov Disord
JT  - Movement disorders : official journal of the Movement Disorder Society
JID - 8610688
OTO - NOTNLM
OT  - MAPT
OT  - N279K mutation
OT  - frontotemporal dementia
OT  - tau PET
EDAT- 2019/02/19 06:00
MHDA- 2019/02/19 06:00
CRDT- 2019/02/19 06:00
PHST- 2018/06/14 00:00 [received]
PHST- 2018/12/08 00:00 [revised]
PHST- 2019/01/02 00:00 [accepted]
PHST- 2019/02/19 06:00 [pubmed]
PHST- 2019/02/19 06:00 [medline]
PHST- 2019/02/19 06:00 [entrez]
AID - 10.1002/mds.27623 [doi]
PST - ppublish
SO  - Mov Disord. 2019 Apr;34(4):568-574. doi: 10.1002/mds.27623. Epub 2019 Feb 17.

PMID- 30788854
OWN - NLM
STAT- In-Data-Review
LR  - 20190315
IS  - 1531-8257 (Electronic)
IS  - 0885-3185 (Linking)
VI  - 34
IP  - 3
DP  - 2019 Mar
TI  - Early distinction of Parkinson-variant multiple system atrophy from Parkinson's
      disease.
PG  - 440-441
LID - 10.1002/mds.27635 [doi]
FAU - Fanciulli, Alessandra
AU  - Fanciulli A
AUID- ORCID: https://orcid.org/0000-0002-2854-4179
AD  - Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
FAU - Goebel, Georg
AU  - Goebel G
AD  - Department of Medical Statistics, Informatics and Health Economics, Medical
      University of Innsbruck, Innsbruck, Austria.
FAU - Lazzeri, Giulia
AU  - Lazzeri G
AD  - IRCCS Foundation Ca' Grande Ospedale Maggiore Policlinico, Dino Ferrari Center,
      Neuroscience Section, Department of Pathophysiology and Transplantation,
      University of Milan, Milan, Italy.
FAU - Scherfler, Christoph
AU  - Scherfler C
AD  - Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
FAU - Gizewski, Elke R
AU  - Gizewski ER
AD  - Department of Neuroradiology, Medical University of Innsbruck, Innsbruck,
      Austria.
FAU - Granata, Roberta
AU  - Granata R
AD  - Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
FAU - Kiss, Gusztav
AU  - Kiss G
AD  - Department of Urology, Medical University of Innsbruck, Innsbruck, Austria.
FAU - Strano, Stefano
AU  - Strano S
AD  - Department of Heart and Great Vessels "A. Reale", Sapienza University of Rome,
      Rome, Italy.
FAU - Colosimo, Carlo
AU  - Colosimo C
AD  - Department of Neurology, Santa Maria Hospital, Terni, Italy.
FAU - Pontieri, Francesco E
AU  - Pontieri FE
AUID- ORCID: https://orcid.org/0000-0002-8693-8432
AD  - Department of Neuroscience, Mental Health and Sensory Organs, Sapienza University
      of Rome, Rome, Italy.
FAU - Kaufmann, Horacio
AU  - Kaufmann H
AD  - Department of Neurology, Dysautonomia Center, New York University School of
      Medicine, New York, New York, USA.
FAU - Seppi, Klaus
AU  - Seppi K
AD  - Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
FAU - Poewe, Werner
AU  - Poewe W
AD  - Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
FAU - Wenning, Gregor K
AU  - Wenning GK
AD  - Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
LA  - eng
PT  - Letter
DEP - 20190220
PL  - United States
TA  - Mov Disord
JT  - Movement disorders : official journal of the Movement Disorder Society
JID - 8610688
EDAT- 2019/02/23 06:00
MHDA- 2019/02/23 06:00
CRDT- 2019/02/22 06:00
PHST- 2018/08/10 00:00 [received]
PHST- 2018/12/21 00:00 [revised]
PHST- 2019/01/14 00:00 [accepted]
PHST- 2019/02/23 06:00 [pubmed]
PHST- 2019/02/23 06:00 [medline]
PHST- 2019/02/22 06:00 [entrez]
AID - 10.1002/mds.27635 [doi]
PST - ppublish
SO  - Mov Disord. 2019 Mar;34(3):440-441. doi: 10.1002/mds.27635. Epub 2019 Feb 20.

PMID- 30787432
OWN - NLM
STAT- In-Data-Review
LR  - 20190329
IS  - 1759-4766 (Electronic)
IS  - 1759-4758 (Linking)
VI  - 15
IP  - 4
DP  - 2019 Apr
TI  - Clinical Parkinson disease subtyping does not predict pathology.
PG  - 189-190
LID - 10.1038/s41582-019-0153-9 [doi]
FAU - Espay, Alberto J
AU  - Espay AJ
AD  - UC James J. and Joan A. Gardner Family Center for Parkinson's Disease and
      Movement Disorders, UC Gardner Neuroscience Institute, Department of Neurology,
      University of Cincinnati, Cincinnati, OH, USA. alberto.espay@uc.edu.
FAU - Marras, Connie
AU  - Marras C
AD  - Morton and Gloria Shulman Movement Disorders Centre and the Edmond J. Safra
      Program in Parkinson's Disease, Toronto Western Hospital, University of Toronto, 
      Toronto, Ontario, Canada.
LA  - eng
PT  - Journal Article
PL  - England
TA  - Nat Rev Neurol
JT  - Nature reviews. Neurology
JID - 101500072
EDAT- 2019/02/23 06:00
MHDA- 2019/02/23 06:00
CRDT- 2019/02/22 06:00
PHST- 2019/02/23 06:00 [pubmed]
PHST- 2019/02/23 06:00 [medline]
PHST- 2019/02/22 06:00 [entrez]
AID - 10.1038/s41582-019-0153-9 [doi]
AID - 10.1038/s41582-019-0153-9 [pii]
PST - ppublish
SO  - Nat Rev Neurol. 2019 Apr;15(4):189-190. doi: 10.1038/s41582-019-0153-9.

PMID- 30778210
OWN - NLM
STAT- In-Data-Review
LR  - 20190329
IS  - 1759-4766 (Electronic)
IS  - 1759-4758 (Linking)
VI  - 15
IP  - 4
DP  - 2019 Apr
TI  - Long-term outcomes of deep brain stimulation in Parkinson disease.
PG  - 234-242
LID - 10.1038/s41582-019-0145-9 [doi]
AB  - The efficacy of deep brain stimulation (DBS) for Parkinson disease (PD) is well
      established for up to 1 or 2 years, but long-term outcome data are still limited.
      In this Review, we critically discuss the evidence on the long-term outcomes of
      DBS and consider the clinical implications. Although many patients are lost to
      follow-up, the evidence indicates that subthalamic nucleus DBS improves motor
      function for up to 10 years, although the magnitude of improvement tends to
      decline over time. Functional scores recorded during on-medication periods worsen
      more quickly than those recorded in off periods, consistent with the degeneration
      of non-dopaminergic pathways. Dyskinesia, motor fluctuations and activities of
      daily living in off periods remain improved at 5 years, but quality-of-life
      scores have usually fallen below preoperative levels. The incidence and severity 
      of dementia among patients receiving DBS are comparable to those among patients
      who receive medical treatment. Severe adverse events are rare, but adverse events
      such as dysarthria are common and probably under-reported. Long-term data on the 
      outcomes of globus pallidus interna DBS are limited and mostly confirm the
      efficacy for dyskinesia. A trend towards offering DBS in the earlier stages of PD
      creates a need to identify factors that predict long-term outcomes and to discuss
      realistic expectations with patients preoperatively.
FAU - Limousin, Patricia
AU  - Limousin P
AUID- ORCID: http://orcid.org/0000-0001-5668-5545
AD  - Department of Clinical and Movement Neurosciences, University College London,
      Queen Square Institute of Neurology, London, UK. p.limousin@ucl.ac.uk.
AD  - National Hospital for Neurology and Neurosurgery, Queen Square, London, UK.
      p.limousin@ucl.ac.uk.
FAU - Foltynie, Tom
AU  - Foltynie T
AD  - Department of Clinical and Movement Neurosciences, University College London,
      Queen Square Institute of Neurology, London, UK.
AD  - National Hospital for Neurology and Neurosurgery, Queen Square, London, UK.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Nat Rev Neurol
JT  - Nature reviews. Neurology
JID - 101500072
EDAT- 2019/02/20 06:00
MHDA- 2019/02/20 06:00
CRDT- 2019/02/20 06:00
PHST- 2019/02/20 06:00 [pubmed]
PHST- 2019/02/20 06:00 [medline]
PHST- 2019/02/20 06:00 [entrez]
AID - 10.1038/s41582-019-0145-9 [doi]
AID - 10.1038/s41582-019-0145-9 [pii]
PST - ppublish
SO  - Nat Rev Neurol. 2019 Apr;15(4):234-242. doi: 10.1038/s41582-019-0145-9.

PMID- 30777766
OWN - NLM
STAT- Publisher
LR  - 20190219
IS  - 1931-1559 (Electronic)
IS  - 0894-4105 (Linking)
DP  - 2019 Feb 18
TI  - Sex, dopamine, and hypokinesia: A study of inflectional morphology in Parkinson's
      disease.
LID - 10.1037/neu0000533 [doi]
AB  - OBJECTIVE: Parkinson's disease (PD), which involves the degeneration of
      dopaminergic basal ganglia neurons, appears to affect language. We investigated
      which aspects of language are impaired in PD and what moderates these
      impairments. Our predictions were based on the declarative/procedural model of
      language, which links grammar, including in regular inflection, to procedural
      memory and left-lateralized basal ganglia dopaminergic circuits but links lexical
      memory, including irregulars, to declarative memory. Because females tend to show
      declarative memory advantages as compared to males, the model predicts that
      females rely more on this system for regulars, which can be stored as chunks.
      METHOD: We probed regular/irregular Farsi past-tense production in 40
      Farsi-speaking patients with moderate-to-severe nondemented PD (half female) and 
      40 normal controls (half female). RESULTS: Consistent with our predictions, we
      found that male, but not female, PD patients showed greater deficits at regular
      than irregular past-tense production. The females' impairment was mildest for
      regulars, likely from compensatory storage, as revealed by regular past-tense
      frequency effects only in females. Right-side hypokinesia (linked to left basal
      ganglia degeneration) correlated negatively with accuracy of regulars but not
      irregulars. Similarly, the levodopa equivalent dose of patients' last medication 
      correlated only with regulars. CONCLUSIONS: The results suggest that language is 
      impaired in PD, but the impairments are moderated by multiple factors, including 
      the type of linguistic knowledge, the degree of left basal ganglia degeneration, 
      dopamine, and sex. The findings underscore the impact of sex on the
      neurocognition of language and the roles of left basal ganglia dopaminergic
      circuits in aspects of rule-governed grammar. (PsycINFO Database Record (c) 2019 
      APA, all rights reserved).
FAU - Johari, Karim
AU  - Johari K
AD  - Speech Neuroscience Lab.
FAU - Walenski, Matthew
AU  - Walenski M
AD  - The Roxelyn and Richard Pepper Department of Communication Sciences and
      Disorders.
FAU - Reifegerste, Jana
AU  - Reifegerste J
AD  - Brain and Language Laboratory.
FAU - Ashrafi, Farzad
AU  - Ashrafi F
AD  - Department of Neurology.
FAU - Ullman, Michael T
AU  - Ullman MT
AD  - Brain and Language Laboratory.
LA  - eng
GR  - National Science Foundation
GR  - National Institute of Health
GR  - Mabel H. Flory Trust
GR  - Tabriz University of Medical Sciences
GR  - Shahid Beheshti University of Medical Sciences
PT  - Journal Article
DEP - 20190218
PL  - United States
TA  - Neuropsychology
JT  - Neuropsychology
JID - 8904467
EDAT- 2019/02/20 06:00
MHDA- 2019/02/20 06:00
CRDT- 2019/02/20 06:00
PHST- 2019/02/20 06:00 [entrez]
PHST- 2019/02/20 06:00 [pubmed]
PHST- 2019/02/20 06:00 [medline]
AID - 2019-08240-001 [pii]
AID - 10.1037/neu0000533 [doi]
PST - aheadofprint
SO  - Neuropsychology. 2019 Feb 18. pii: 2019-08240-001. doi: 10.1037/neu0000533.

PMID- 29567422
OWN - NLM
STAT- MEDLINE
DCOM- 20190222
LR  - 20190222
IS  - 1872-7972 (Electronic)
IS  - 0304-3940 (Linking)
VI  - 675
DP  - 2018 May 14
TI  - Neuroprotective effect of IDPU (1-(7-imino-3-propyl-2,3-dihydrothiazolo
      [4,5-d]pyrimidin-6(7H)-yl)urea) in 6-OHDA induced rodent model of hemiparkinson's
      disease.
PG  - 74-82
LID - S0304-3940(18)30217-9 [pii]
LID - 10.1016/j.neulet.2018.03.040 [doi]
AB  - Parkinson's disease (PD) is a progressive neurodegenerative motor disorder
      characterized by the degeneration of dopaminergic nigrostriatal neurons. Levodopa
      (l-DOPA) is the most effective therapy for PD, however, PD progression continues 
      with significant side effects in long term, thus necessitating the search for
      effective therapy that impedes PD progression. PD therapy through
      non-dopaminergic pathways offers treatment without the risk of extrapyramidal
      effects. In this regard, earlier, we had reported, a novel compound IDPU with
      potential adenosine A2A receptor antagonist effect in haloperidol (chronic
      treatment) induced Parkinson model. In the present study, we extended our
      investigation towards i) evaluation of IDPU in well-established 6-OHDA induced
      Parkinson rat model to establish its role in the therapy of PD ii) its function
      in alleviating the neuronal loss. We carried the IDPU administration (i.p.) in
      rats for two weeks after establishing 6-OHDA induced unilateral lesions. The
      behavioral activity, neurochemical alteration, oxidative stress marker and
      tyrosine hydroxylase positive neurons in substantia nigra were analyzed. The
      results showed that IDPU significantly reduced motor and non-motor deficits
      induced by 6-OHDA in the behavioral tasks such as apomorphine, rota rod and force
      swim test. Furthermore, the results of oxidative stress biomarkers revealed that 
      IDPU successfully modulated oxidative stress associated biomarkers such as MDA,
      catalase, superoxide dismutase, nitric oxide and reduced glutathione level.
      Additionally, IDPU significantly elevated intracellular dopamine, decreased
      glutamate and calcium levels in brain as compared to 6-OHDA alone treated animals
      which is evocative of its neuroprotective behavior. Thus, the investigations
      clearly validated IDPU as a potent anti-parkinsonian agent which showed immense
      capability to protect neurodegeneration.
CI  - Copyright (c) 2018 Elsevier B.V. All rights reserved.
FAU - Kumari, Namrata
AU  - Kumari N
AD  - Dr. B.R. Ambedkar Center for Biomedical Research, University of Delhi, New Delhi,
      India.
FAU - Agrawal, Saurabh
AU  - Agrawal S
AD  - Dr. B.R. Ambedkar Center for Biomedical Research, University of Delhi, New Delhi,
      India.
FAU - Kumari, Rita
AU  - Kumari R
AD  - Dr. B.R. Ambedkar Center for Biomedical Research, University of Delhi, New Delhi,
      India.
FAU - Sharma, Dimpy
AU  - Sharma D
AD  - Dr. B.R. Ambedkar Center for Biomedical Research, University of Delhi, New Delhi,
      India.
FAU - Luthra, Pratibha Mehta
AU  - Luthra PM
AD  - Dr. B.R. Ambedkar Center for Biomedical Research, University of Delhi, New Delhi,
      India. Electronic address: pmluthra@acbr.du.ac.in.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180319
PL  - Ireland
TA  - Neurosci Lett
JT  - Neuroscience letters
JID - 7600130
RN  - 0 ((1-(7-imino-3-propyl-2,3-dihydrothiazolo(4,5-d)pyrimidin-6(7H)-yl)urea)
RN  - 0 (Antiparkinson Agents)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Thiazoles)
RN  - 8HW4YBZ748 (Oxidopamine)
RN  - 8W8T17847W (Urea)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
SB  - IM
MH  - Animals
MH  - Antiparkinson Agents/*administration & dosage
MH  - Behavior, Animal/drug effects
MH  - Depression
MH  - Disease Models, Animal
MH  - Male
MH  - Neuroprotective Agents/*administration & dosage
MH  - Oxidopamine/administration & dosage
MH  - Parkinson Disease/metabolism/*prevention & control
MH  - Parkinsonian Disorders/chemically induced/metabolism/prevention & control
MH  - Rats, Wistar
MH  - Reactive Oxygen Species/metabolism
MH  - Rotarod Performance Test
MH  - Thiazoles/*administration & dosage
MH  - Tyrosine 3-Monooxygenase/metabolism
MH  - Urea/administration & dosage/*analogs & derivatives
OTO - NOTNLM
OT  - *6-OHDA
OT  - *A(2A) receptor antagonist
OT  - *Parkinson's disease
EDAT- 2018/03/24 06:00
MHDA- 2019/02/23 06:00
CRDT- 2018/03/24 06:00
PHST- 2017/12/03 00:00 [received]
PHST- 2018/03/02 00:00 [revised]
PHST- 2018/03/18 00:00 [accepted]
PHST- 2018/03/24 06:00 [pubmed]
PHST- 2019/02/23 06:00 [medline]
PHST- 2018/03/24 06:00 [entrez]
AID - S0304-3940(18)30217-9 [pii]
AID - 10.1016/j.neulet.2018.03.040 [doi]
PST - ppublish
SO  - Neurosci Lett. 2018 May 14;675:74-82. doi: 10.1016/j.neulet.2018.03.040. Epub
      2018 Mar 19.

PMID- 29203207
OWN - NLM
STAT- MEDLINE
DCOM- 20190218
LR  - 20190219
IS  - 1872-7972 (Electronic)
IS  - 0304-3940 (Linking)
VI  - 672
DP  - 2018 Apr 13
TI  - Suppression of autophagy in the brain of transgenic mice with overexpression of
      capital A, Cyrillic53capital TE, Cyrillic-mutant alpha-synuclein as an early
      event at synucleinopathy progression.
PG  - 140-144
LID - S0304-3940(17)30974-6 [pii]
LID - 10.1016/j.neulet.2017.12.001 [doi]
AB  - Transgenic overexpression of alpha-synuclein is a common model of Parkinson's
      disease (PD). Accumulation of capital A, Cyrillic53capital TE, Cyrillic-mutant
      alpha-synuclein induces three autophagy cell responses: the inhibition of
      autophagy caused by the accumulation of alpha-synuclein, compensatory activation 
      of macroautophagy in response to inhibition of the chaperone-mediated autophagy, 
      and toxic effects of mutant alpha-synuclein accompanied by the activation of
      autophagy. The overall effect of long-term overexpression of mutant
      alpha-synuclein in vivo remains unclear. Here we evaluated the activity of
      autophagy in the frontal cortex, striatum and s.nigra of transgenic mice with
      overexpression of capital A, Cyrillic53capital TE, Cyrillic-mutant
      alpha-synuclein. We revealed low autophagic activity in the dopaminergic
      structures of 5mo. transgenic B6.Cg-Tg(Prnp-SNCA*A53T)23Mkle/J mice as compared
      to controls C57Bl/6J mice. The results were further supported by the data on
      tyrosine hydroxylase immunostaining that indicated its significant decrease in
      the striatum but not in s.nigra of transgenic mice and might be more related to
      earlier damage of dopaminergic neurites than to the somas due to disturbed
      formation of autophagosomes at the neuron periphery. The results provide evidence
      of a possible contribution of suppressed autophagy to the development of PD-like 
      condition as an early event at synucleinopathy progression. Activation of
      autophagy at early stages of PD seems to be a promising therapeutic tool while
      B6.Cg-Tg(Prnp-SNCA*A53T)23Mkle/J mice are suggested as a suitable and adequate
      model for studying the neuroprotective potential and value of this approach.
CI  - Copyright (c) 2017 Elsevier B.V. All rights reserved.
FAU - Pupyshev, Alexander B
AU  - Pupyshev AB
AD  - Federal State Budgetary Scientific Institution "Scientific Research Institute of 
      Physiology and Basic Medicine" (SRIPhBM), Novosibirsk 630117, Russia. Electronic 
      address: pupyshevab@physiol.ru.
FAU - Korolenko, Tatiana A
AU  - Korolenko TA
AD  - Federal State Budgetary Scientific Institution "Scientific Research Institute of 
      Physiology and Basic Medicine" (SRIPhBM), Novosibirsk 630117, Russia.
FAU - Akopyan, Anna A
AU  - Akopyan AA
AD  - Federal State Budgetary Scientific Institution "Scientific Research Institute of 
      Physiology and Basic Medicine" (SRIPhBM), Novosibirsk 630117, Russia.
FAU - Amstislavskaya, Tamara G
AU  - Amstislavskaya TG
AD  - Federal State Budgetary Scientific Institution "Scientific Research Institute of 
      Physiology and Basic Medicine" (SRIPhBM), Novosibirsk 630117, Russia; Novosibirsk
      State University, Novosibirsk 630090, Russia.
FAU - Tikhonova, Maria A
AU  - Tikhonova MA
AD  - Federal State Budgetary Scientific Institution "Scientific Research Institute of 
      Physiology and Basic Medicine" (SRIPhBM), Novosibirsk 630117, Russia; Novosibirsk
      State University, Novosibirsk 630090, Russia.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171202
PL  - Ireland
TA  - Neurosci Lett
JT  - Neuroscience letters
JID - 7600130
RN  - 0 (alpha-Synuclein)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
SB  - IM
MH  - Animals
MH  - Autophagy/*genetics
MH  - Corpus Striatum/*metabolism
MH  - Disease Models, Animal
MH  - Disease Progression
MH  - Dopaminergic Neurons/metabolism
MH  - Frontal Lobe/*metabolism
MH  - Mice
MH  - Mice, Transgenic
MH  - Parkinson Disease/*genetics/metabolism
MH  - Substantia Nigra/*metabolism
MH  - Tyrosine 3-Monooxygenase/metabolism
MH  - alpha-Synuclein/*genetics/metabolism
OTO - NOTNLM
OT  - *Animal model
OT  - *Autophagy
OT  - *LC3-II
OT  - *Mouse
OT  - *Parkinson's disease
OT  - *capital A, Cyrillic53capital TE, Cyrillic-mutant alpha-synuclein
EDAT- 2017/12/06 06:00
MHDA- 2019/02/20 06:00
CRDT- 2017/12/06 06:00
PHST- 2017/09/14 00:00 [received]
PHST- 2017/11/08 00:00 [revised]
PHST- 2017/12/01 00:00 [accepted]
PHST- 2017/12/06 06:00 [pubmed]
PHST- 2019/02/20 06:00 [medline]
PHST- 2017/12/06 06:00 [entrez]
AID - S0304-3940(17)30974-6 [pii]
AID - 10.1016/j.neulet.2017.12.001 [doi]
PST - ppublish
SO  - Neurosci Lett. 2018 Apr 13;672:140-144. doi: 10.1016/j.neulet.2017.12.001. Epub
      2017 Dec 2.

PMID- 29030221
OWN - NLM
STAT- MEDLINE
DCOM- 20190222
LR  - 20190222
IS  - 1872-7972 (Electronic)
IS  - 0304-3940 (Linking)
VI  - 675
DP  - 2018 May 14
TI  - Inhibition of BDNF production by MPP(+) through up-regulation of miR-210-3p
      contributes to dopaminergic neuron damage in MPTP model.
PG  - 133-139
LID - S0304-3940(17)30832-7 [pii]
LID - 10.1016/j.neulet.2017.10.014 [doi]
AB  - The neurotrophin brain-derived neurotrophic factor (BDNF) has been involved in
      supporting of neuron survival. The observation of reduced level of BDNF in the
      substantia nigra (SN) of Parkinson's disease (PD) patients suggests its important
      role in neuron protection in PD pathogenesis. However, the mechanism underlying
      the down-regulation of BDNF in PD was largely unknown. In this study, we found
      that miR-210-3p is involved in the regulation of BDNF production by
      1-methyl-4-phenylpyridinium (MPP(+)). MPP(+) inhibits the BDNF production in
      SH-SY5Y cells through a transcription independent manner. Moreover, miR-210-3p,
      which targets BDNF mRNA, is up-regulated by MPP(+) in SH-SY5Y cells. Importantly,
      inhibition of miR-210-3p prevents the reduction of BDNF production by MPP(+) and 
      improves the DA neuron survival in 1-methyl-4-phenyl-1,2,3,6-tetra hydropyridine 
      (MPTP) model. Together, we demonstrated up-regulation of miR-210-3p by MPP(+)
      reduces the BDNF production and contributes to the DA neuron damage.
CI  - Copyright (c) 2017. Published by Elsevier B.V.
FAU - Zhang, Shan
AU  - Zhang S
AD  - Department of Neurology, The People's Hospital of Leshan, Leshan 614000, Sichuan,
      China.
FAU - Chen, Shu
AU  - Chen S
AD  - Department of Neurosurgery, The People's Hospital of Leshan, Leshan 614000,
      Sichuan, China.
FAU - Liu, Anmin
AU  - Liu A
AD  - Department of Neurosurgery, SunYat-sen Memorial Hospital, SunYat-sen University, 
      Guangzhou 510120, Guangdong, China.
FAU - Wan, Jungang
AU  - Wan J
AD  - Department of Neurology, The People's Hospital of Leshan, Leshan 614000, Sichuan,
      China.
FAU - Tang, Lingwen
AU  - Tang L
AD  - Department of Neurology, The People's Hospital of Leshan, Leshan 614000, Sichuan,
      China.
FAU - Zheng, Niandong
AU  - Zheng N
AD  - Department of Neurosurgery, The People's Hospital of Leshan, Leshan 614000,
      Sichuan, China.
FAU - Xiong, Yi
AU  - Xiong Y
AD  - Department of Neurology, The People's Hospital of Leshan, Leshan 614000, Sichuan,
      China. Electronic address: xiongyixiaoyan@163.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171013
PL  - Ireland
TA  - Neurosci Lett
JT  - Neuroscience letters
JID - 7600130
RN  - 0 (Bdnf protein, mouse)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (MIRN210 microRNA, human)
RN  - 0 (MIRN210 microRNA, mouse)
RN  - 0 (MicroRNAs)
RN  - 7171WSG8A2 (BDNF protein, human)
RN  - R865A5OY8J (1-Methyl-4-phenylpyridinium)
SB  - IM
MH  - 1-Methyl-4-phenylpyridinium/*administration & dosage
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Cell Line, Tumor
MH  - Dopaminergic Neurons/drug effects/*metabolism/pathology
MH  - Down-Regulation
MH  - Humans
MH  - Mice, Inbred C57BL
MH  - MicroRNAs/*metabolism
MH  - Parkinson Disease/*metabolism
MH  - Parkinsonian Disorders/metabolism
MH  - Up-Regulation
OTO - NOTNLM
OT  - *BDNF
OT  - *MPP(+)
OT  - *Neuron damage
OT  - *Parkinson's disease
OT  - *miR-210-3p
EDAT- 2017/10/17 06:00
MHDA- 2019/02/23 06:00
CRDT- 2017/10/15 06:00
PHST- 2017/04/25 00:00 [received]
PHST- 2017/10/08 00:00 [revised]
PHST- 2017/10/09 00:00 [accepted]
PHST- 2017/10/17 06:00 [pubmed]
PHST- 2019/02/23 06:00 [medline]
PHST- 2017/10/15 06:00 [entrez]
AID - S0304-3940(17)30832-7 [pii]
AID - 10.1016/j.neulet.2017.10.014 [doi]
PST - ppublish
SO  - Neurosci Lett. 2018 May 14;675:133-139. doi: 10.1016/j.neulet.2017.10.014. Epub
      2017 Oct 13.

PMID- 30790668
OWN - NLM
STAT- In-Data-Review
LR  - 20190405
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Linking)
VI  - 404
DP  - 2019 Apr 15
TI  - State-Dependent Spike and Local Field Synchronization between the Thalamic
      Parafascicular Nucleus and the Dorsal Striatum in a Rat Model of Parkinson's
      Disease.
PG  - 27-38
LID - S0306-4522(19)30082-X [pii]
LID - 10.1016/j.neuroscience.2019.01.055 [doi]
AB  - Recent studies on the impact of Parkinson's disease (PD) on the thalamostriatal
      pathway have mainly focused on the structural and functional changes in the
      thalamus projection to the striatum. Alterations in the electrophysiological
      activity of the thalamostriatal circuit in PD have not been intensively studied. 
      To further investigate this circuit, parafascicular nucleus (PF) single-unit
      spikes and dorsal striatum local field potential (LFP) activities were
      simultaneously recorded in control and 6-hydroxydopamine (6-OHDA)-lesioned rats
      during inattentive rest or treadmill walking states. We classified the PF neurons
      into two predominant subtypes (PF I and PF II). During rest state, after dopamine
      loss, increased PF I spike and striatal LFP coherence was observed in the
      beta-frequency (12-35Hz), with changed PF I neuronal firing pattern and unchanged
      firing rates of the two neuron subtypes. However, in a treadmill walking state,
      PF II neurons displayed markedly increased coherence to striatal beta
      oscillations in the dopamine-depleted rats, as well as an altered PF II neuronal 
      firing pattern and significantly decreased firing rates of the two neuron
      subtypes. The results indicate that in PD animals, state transition from rest to 
      moving, such as treadmill walking, is associated with different PF neuron types
      and increased spike-LFP synchronization, which may provide new paradigms for
      understanding and treating PD.
CI  - Copyright (c) 2019. Published by Elsevier Ltd.
FAU - Zhang, Haiyan
AU  - Zhang H
AD  - Key laboratory of Animal Resistance Biology of Shandong Province, College of Life
      Science, Shandong Normal University, Jinan 250014, People's Republic of China.
FAU - Yang, Jing
AU  - Yang J
AD  - Key laboratory of Animal Resistance Biology of Shandong Province, College of Life
      Science, Shandong Normal University, Jinan 250014, People's Republic of China.
FAU - Xiang, Tianyu
AU  - Xiang T
AD  - Key laboratory of Animal Resistance Biology of Shandong Province, College of Life
      Science, Shandong Normal University, Jinan 250014, People's Republic of China.
FAU - Sun, Shuang
AU  - Sun S
AD  - Key laboratory of Animal Resistance Biology of Shandong Province, College of Life
      Science, Shandong Normal University, Jinan 250014, People's Republic of China.
FAU - Wang, Xiusong
AU  - Wang X
AD  - Key laboratory of Animal Resistance Biology of Shandong Province, College of Life
      Science, Shandong Normal University, Jinan 250014, People's Republic of China.
FAU - Wang, Xuenan
AU  - Wang X
AD  - Key laboratory of Animal Resistance Biology of Shandong Province, College of Life
      Science, Shandong Normal University, Jinan 250014, People's Republic of China.
FAU - Li, Min
AU  - Li M
AD  - Key laboratory of Animal Resistance Biology of Shandong Province, College of Life
      Science, Shandong Normal University, Jinan 250014, People's Republic of China.
FAU - Guo, Mengnan
AU  - Guo M
AD  - Key laboratory of Animal Resistance Biology of Shandong Province, College of Life
      Science, Shandong Normal University, Jinan 250014, People's Republic of China.
FAU - Jia, Qingmei
AU  - Jia Q
AD  - Key laboratory of Animal Resistance Biology of Shandong Province, College of Life
      Science, Shandong Normal University, Jinan 250014, People's Republic of China.
FAU - Chen, Dadian
AU  - Chen D
AD  - Key laboratory of Animal Resistance Biology of Shandong Province, College of Life
      Science, Shandong Normal University, Jinan 250014, People's Republic of China.
FAU - Wang, Min
AU  - Wang M
AD  - Key laboratory of Animal Resistance Biology of Shandong Province, College of Life
      Science, Shandong Normal University, Jinan 250014, People's Republic of China.
      Electronic address: wangmin@sdnu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20190219
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
OTO - NOTNLM
OT  - Parkinson's disease
OT  - dorsal striatum
OT  - parafascicular thalamic nucleus
OT  - synchronization
EDAT- 2019/02/23 06:00
MHDA- 2019/02/23 06:00
CRDT- 2019/02/22 06:00
PHST- 2018/09/26 00:00 [received]
PHST- 2019/01/26 00:00 [revised]
PHST- 2019/01/28 00:00 [accepted]
PHST- 2019/02/23 06:00 [pubmed]
PHST- 2019/02/23 06:00 [medline]
PHST- 2019/02/22 06:00 [entrez]
AID - S0306-4522(19)30082-X [pii]
AID - 10.1016/j.neuroscience.2019.01.055 [doi]
PST - ppublish
SO  - Neuroscience. 2019 Apr 15;404:27-38. doi: 10.1016/j.neuroscience.2019.01.055.
      Epub 2019 Feb 19.