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Perry Syndrome

, MD and , MD.

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Initial Posting: ; Last Update: September 29, 2016.

Estimated reading time: 18 minutes


Clinical characteristics.

Perry syndrome is characterized by parkinsonism, hypoventilation, depression, and weight loss. The mean age at onset is 49 years; the mean disease duration is five years. Parkinsonism and psychiatric changes (depression, apathy, character changes, and withdrawal) tend to occur early; severe weight loss and hypoventilation manifest later.


The diagnosis of Perry syndrome is established in a proband with all four of the cardinal features:

  • Early-onset familial parkinsonism
  • Mood/personality changes
  • Weight loss
  • Central hypoventilation

Identification of a heterozygous DCTN1 pathogenic variant on molecular genetic testing confirms the diagnosis if clinical features are inconclusive.


Treatment of manifestations: Dopaminergic therapy (particularly carbidopa/levodopa) should be considered in all individuals with significant parkinsonism. Although response to levodopa is often poor, some individuals may have long-term benefit. At times large doses of carbidopa/levodopa are required. Ventilation support may prolong life expectancy and improve quality of life. Those individuals with psychiatric manifestations may benefit from antidepressants and psychiatric care. Weight loss is managed with appropriate dietary changes.

Prevention of secondary complications: Adequate caloric intake to prevent weight loss.

Surveillance: Routine evaluation of weight and calorie intake, respiratory function (particularly at night or during sleep), motor function, and mood/personality changes.

Agents/circumstances to avoid: Central respiratory depressants (e.g., benzodiazepines, alcohol, narcotics).

Genetic counseling.

Perry syndrome is inherited in an autosomal dominant manner. The proportion of cases attributed to a de novo pathogenic variant is unknown. Each child of an individual with Perry syndrome has a 50% chance of inheriting the pathogenic variant. Prenatal and preimplantation genetic testing are possible for families in which the pathogenic variant has been identified.


Suggestive Findings

Perry syndrome should be suspected in individuals with these cardinal clinical features:

  • Early-onset familial parkinsonism
  • Mood/personality changes (depression, apathy, withdrawal, disinhibition)
  • Weight loss
  • Central hypoventilation

Diagnostic criteria were previously proposed prior to the availability of molecular and immunohistochemistry testing [Wider & Wszolek 2008]. However, with the availability of molecular genetic testing they are no longer crucial for the diagnosis.

Establishing the Diagnosis

The diagnosis of Perry syndrome can be established in a proband who has ALL of the above cardinal features.

Identification of a heterozygous DCTN1 pathogenic variant on molecular genetic testing confirms the diagnosis if clinical features are inconclusive (see Table 1). Molecular testing approaches can include single-gene testing, use of a multigene panel, and more comprehensive genomic testing.

  • Single-gene testing. Perform sequence analysis of DCTN1.
    Note: Since Perry syndrome occurs through a dominant-negative mechanism (see Molecular Genetics) and large intragenic deletion or duplication has not been reported, testing for intragenic deletions or duplication is unlikely to identify a disease-causing variant. Detailed genetic studies for intragenic deletions or duplications have not been conducted.
  • A multigene panel that includes DCTN1 and other genes of interest (see Differential Diagnosis) may also be considered. Note: (1) The genes included in the panel and the diagnostic sensitivity of the testing used for each gene vary by laboratory and are likely to change over time. (2) Some multigene panels may include genes not associated with the condition discussed in this GeneReview; thus, clinicians need to determine which multigene panel is most likely to identify the genetic cause of the condition at the most reasonable cost while limiting identification of variants of uncertain significance and pathogenic variants in genes that do not explain the underlying phenotype. (3) In some laboratories, panel options may include a custom laboratory-designed panel and/or custom phenotype-focused exome analysis that includes genes specified by the clinician. (4) Methods used in a panel may include sequence analysis, deletion/duplication analysis, and/or other non-sequencing-based tests.
    For an introduction to multigene panels click here. More detailed information for clinicians ordering genetic tests can be found here.
  • More comprehensive genomic testing (when available) including exome sequencing and genome sequencing may be considered if serial single-gene testing (and/or use of a multigene panel that includes DCTN1) fails to confirm a diagnosis in an individual with features of Perry syndrome. Such testing may provide or suggest a diagnosis not previously considered (e.g., mutation of a different gene or genes that results in a similar clinical presentation). For an introduction to comprehensive genomic testing click here. More detailed information for clinicians ordering genomic testing can be found here.

Table 1.

Molecular Genetic Testing Used in Perry syndrome

Gene 1MethodProportion of Probands with a Pathogenic Variant 2 Detectable by Method
DCTN1Sequence analysis 321/21 (100%) 4
Gene-targeted deletion/duplication analysis 5Unknown 6

See Molecular Genetics for information on allelic variants detected in this gene.


Sequence analysis detects variants that are benign, likely benign, of uncertain significance, likely pathogenic, or pathogenic. Variants may include small intragenic deletions/insertions and missense, nonsense, and splice site variants; typically, exon or whole-gene deletions/duplications are not detected. For issues to consider in interpretation of sequence analysis results, click here.


Gene-targeted deletion/duplication analysis detects intragenic deletions or duplications. Methods used may include quantitative PCR, long-range PCR, multiplex ligation-dependent probe amplification (MLPA), and a gene-targeted microarray designed to detect single-exon deletions or duplications.


Since Perry syndrome occurs through a dominant-negative mechanism and large intragenic deletion or duplication has not been reported, testing for intragenic deletions or duplication is unlikely to identify a disease-causing variant.

Clinical Characteristics

Clinical Description

The cardinal findings of Perry syndrome are parkinsonism, hypoventilation, depression, and weight loss [Wider & Wszolek 2008, Wider et al 2010]. The mean age at onset is 49 years (range: 35-70 years) and the mean disease duration is five years (range: 2-14 years). Psychiatric (depression, apathy, character changes, withdrawal) and motor (parkinsonism) symptoms tend to occur early, whereas severe weight loss and hypoventilation manifest later. In most affected persons the reported cause/circumstance of death relates to sudden death/hypoventilation or suicide [Wider & Wszolek 2008].

Parkinsonism. Most affected individuals present with akinetic-rigid and rather symmetric parkinsonism that is less severe than that found in Parkinson disease. When present, tremor is often postural; however, typical rest tremor has been reported.

Hypoventilation. Alveolar hypoventilation manifests particularly at night or during sleep with tachypnea alternating with normal respiratory cycles, leading to frequent awakenings. Polysomnographic recordings show that hypoxemia and hypercapnia are of central origin; that is, there is no obstructive or structural respiratory tract abnormality. One detailed autopsy study demonstrated significant neuronal loss in regions critical for respiratory drive (ventrolateral medulla [pre-Bötzinger complex] and dorsal raphe nucleus), which may account for central hypoventilation [Tsuboi et al 2008]. Of note, hypoventilation was not reported in one of the ten families with molecularly confirmed Perry syndrome [Roy et al 1988, Farrer et al 2009].

Sleep difficulties, a common complaint, reflect hypoventilation.

Depression. Psychiatric findings are dominated by apathy, social withdrawal, and "loss of psychic self-activation" (referred to as "athymhormia" in the French literature), although true depression has also been reported.

One affected individual also presented with frontotemporal dementia-type behavioral manifestations, downward gaze abnormalities, and autonomic dysfunction [Newsway et al 2010].

Weight loss. No anatomic substrate has been reported to account for severe weight loss. Additionally, in most affected individuals weight loss cannot be attributed to significant dysphagia. Weight loss may in fact reflect psychiatric changes; however, mechanisms involving central modification of hunger sensation or an increase in metabolic rate cannot be excluded.

Autonomic failure. In one family from Japan with a DCTN1 pathogenic variant, the four affected individuals displayed early and severe autonomic failure [Ohshima et al 2010].


  • Structural brain imaging is usually normal.
  • Functional imaging using 18-fluorodeoxyglucose PET (FDG-PET) showed reduced metabolic rate in the lateral prefrontal and temporal regions in one study [Lechevalier et al 2005].
  • Dopaminergic pathway functional imaging using 18-fluorodopa PET (FD-PET) showed reduced striatal tracer uptake [Perry et al 1990, Felicio et al 2014]. The tracer reduction uptake was also observed to a lesser extent in an individual with a DCTN1 pathogenic variant who did not have clinical features of Perry syndrome [Felicio et al 2014].
  • Serotonin transporter imaging using 11C-3-amino-4-(2-dimethylaminomethyl-phenylsulfanyl)-benzonitrile (DASB-PET) showed reduced tracer uptake in cortical and subcortical regions [Felicio et al 2014].
  • Transcranial sonography showed hyperechogenicity in the substantia nigra comparable to that observed in Parkinson disease [Saka et al 2010].
  • In four affected individuals in one family from Japan, decreased cardiac uptake with [123]-metaiodobenzylguanidine scintigram was reported [Ohshima et al 2010].

Neuropathology. Histology shows severe neuronal loss in the substantia nigra, with no Lewy bodies. Lesser degrees of neuronal loss are found in the locus ceruleus, lentiform nucleus, hypothalamus, periaqueductal gray matter, dorsal raphe nucleus, and brain stem reticular formation [Wider et al 2009]. Specific loss of putative respiratory neurons was demonstrated in the ventrolateral medulla and dorsal raphe nucleus [Tsuboi et al 2008].

Immunohistochemistry shows ubiquitin- and transactive response DNA-binding protein 43 (TDP-43)-positive neuronal inclusions, dystrophic neurites, glial cytoplasmic inclusions, and axonal spheroids [Wider et al 2009]. TDP-43-positive inclusions predominate in regions belonging to the extrapyramidal system including the substantia nigra, globus pallidus, striatum, and subthalamic nucleus. Interestingly, TDP-43-positive inclusions in persons with Perry syndrome resemble those found in ubiquitin-positive frontotemporal lobar degeneration (FTLD-U) and amyotrophic lateral sclerosis (ALS), although with distinct regional distributions.

Genotype-Phenotype Correlations

Eight pathogenic variants in DCTN1 have been associated with Perry syndrome (see Table 2) [Farrer et al 2009, Aji et al 2013, Araki et al 2014, Chung et al 2014, Tacik et al 2014]. No clear genotype-phenotype correlation exists, in that families/individuals with the same pathogenic variant in DCTN1 do not necessarily share the same phenotype.

Persons with Perry syndrome may not develop all of the cardinal manifestations. For example, individuals from the same family may not have hypoventilation and weight loss, and others may lack psychiatric symptoms [Wider et al 2010].


Although precise estimates have not been calculated given the limited number of families reported, penetrance is age related and high, with all asymptomatic heterozygotes being younger than or within the range of onset age.


Before Perry syndrome became the prevailing term for the disorder, several terms had been used to describe this condition, including hereditary mental depression and parkinsonism with taurine deficiency [Perry et al 1975], familial fatal parkinsonism with alveolar hypoventilation and mental depression [Purdy et al 1979], familial parkinsonism, apathy, weight loss, and central hypoventilation [Roy et al 1988], dominantly inherited apathy, central hypoventilation, and Parkinson’s syndrome [Perry et al 1990], familial parkinsonism with athymhormia and hypoventilation [Lechevalier et al 1992], familial parkinsonism with depression [Bhatia et al 1993], and familial parkinsonism with apathy, depression, and central hypoventilation [Elibol et al 2002].

"Perry syndrome" has appeared in the literature since 2002 [Elibol et al 2002]; it is named after Professor Thomas L Perry, who reported the first Canadian family with this disease.


Since the original reports of Perry et al [1975] and Perry et al [1990], 21 additional families have been reported from Canada, the United States, the United Kingdom, Japan, France, Turkey, New Zealand, Colombia, Korea, Portugal, and Taiwan [Purdy et al 1979, Roy et al 1988, Lechevalier et al 1992, Tsuboi et al 2002, Lechevalier et al 2005, Wider & Wszolek 2008, Newsway et al 2010, Ohshima et al 2010, Saka et al 2010, Wider et al 2010, Aji et al 2013, Chung et al 2014, Pretelt et al 2014, Tacik et al 2014, Araki et al 2014, Caroppo et al 2014, Barreto et al 2015, Gustavsson et al 2016].

Differential Diagnosis

Other forms of familial early-onset parkinsonism that need to be distinguished from Perry syndrome include those types caused by mutation of PRKN (PARK2) (see Parkin Type of Early-Onset Parkinson Disease), PINK1 (see PINK1 Type of Young-Onset Parkinson Disease), PARK7 (formerly DJ-1), or LRRK2 (see LRRK2-Related Parkinson Disease). The findings of personality changes, weight loss, and hypoventilation in Perry syndrome tend to distinguish it from other forms of early-onset Parkinson disease (see Parkinson Disease Overview). Additionally, response to standard doses of levodopa is usually poorer or of shorter duration in Perry syndrome than in other forms of early-onset Parkinson disease.

Mood/personality changes in Perry syndrome may suggest frontotemporal dementia, which has a similar age of onset and is often associated with levodopa-resistant parkinsonism.

Perry syndrome needs to be distinguished from frontotemporal dementia caused by mutation of MAPT or GRN (see GRN-Related Frontotemporal Dementia). An individual of Japanese ancestry who showed symptoms reminiscent of Perry syndrome was found to have an MAPT pathogenic variant. On autopsy examination, the brain showed tau-positive inclusions; transactive response DNA-binding protein 43 (TDP-43)-positive inclusions were not present [Omoto et al 2012].


Evaluations Following Initial Diagnosis

To establish the extent of disease and needs in an individual diagnosed with Perry syndrome the following evaluations are recommended:

  • Neurologic evaluation of motor function
  • Sleep study and evaluation by a pulmonologist or sleep disorders consultant for ventilation support if required
  • Psychiatric evaluation and (if needed) neuropsychological examination
  • Consultation with a clinical geneticist and/or genetic counselor

Treatment of Manifestations

Parkinsonism. Dopaminergic therapy (particularly carbidopa/levodopa) should be considered in all individuals with significant parkinsonism. Response to levodopa is usually absent, erratic, or transient in Perry syndrome [Tsuboi et al 2002, Wider & Wszolek 2008]. However, large doses of carbidopa/levodopa (>2g) have been used successfully to reduce rigidity, tremor, and other symptoms in two individuals, one from the new British kindred [Newsway et al 2010] and one from the original Canadian family [J Stoessl, personal communication].

Hypoventilation. Ventilation support (invasive or noninvasive) may prolong life expectancy and have a significant impact on quality of life. Several persons without evidence of daytime central hypoventilation or respiratory troubles died suddenly at night most likely as a result of nocturnal hypoventilation. Therefore, ventilation support may be needed only during sleep [Wider & Wszolek, personal observation]. A bilateral diaphragmatic pacemaker may help combat respiratory insufficiency [Pretelt et al 2014].

Depression. Psychiatric manifestations may require antidepressants and psychiatric follow up to help reduce risk of suicide.

Weight loss. Careful weight follow up is indicated and high caloric intake should be considered if weight loss is present.

Prevention of Secondary Complications

Adequate caloric intake must be ensured to prevent weight loss.


Routine evaluation of weight and calorie intake, respiratory function (particularly at night or during sleep), motor function, and mood/personality changes is appropriate.

Agents/Circumstances to Avoid

Use of central respiratory depressants (e.g., benzodiazepines, alcohol, narcotics) should be minimized.

Evaluation of Relatives at Risk

See Genetic Counseling for issues related to testing of at-risk relatives for genetic counseling purposes.

Therapies Under Investigation

Search in the US and EU Clinical Trials Register in Europe for access to information on clinical studies for a wide range of diseases and conditions. Note: There may not be clinical trials for this disorder.

Genetic Counseling

Genetic counseling is the process of providing individuals and families with information on the nature, inheritance, and implications of genetic disorders to help them make informed medical and personal decisions. The following section deals with genetic risk assessment and the use of family history and genetic testing to clarify genetic status for family members. This section is not meant to address all personal, cultural, or ethical issues that individuals may face or to substitute for consultation with a genetics professional. —ED.

Mode of Inheritance

Perry syndrome is inherited in an autosomal dominant manner.

Risk to Family Members

Parents of a proband

  • Individuals diagnosed with Perry syndrome usually have an affected parent.
  • A proband with Perry syndrome may have the disorder as the result of a de novo DCTN1 pathogenic variant. Because simplex cases (i.e., a single occurrence in a family) have not been evaluated sufficiently to determine if the pathogenic variant was de novo, the proportion of Perry syndrome caused by a de novo pathogenic variant is unknown.
  • If the pathogenic variant found in the proband cannot be detected in leukocyte DNA of either parent, possible explanations include a de novo pathogenic variant in the proband or germline mosaicism in a parent. Although no instances of germline mosaicism have been reported, it remains a possibility.
  • Recommendations for the evaluation of parents of a proband with an apparent de novo pathogenic variant include clinical and genetic evaluations. Evaluation of parents may determine that one is affected but has escaped previous diagnosis because of a milder phenotypic presentation. Therefore, an apparently negative family history cannot be confirmed until appropriate evaluations have been performed.
  • Note: Although most individuals diagnosed with Perry syndrome have an affected parent, the family history may appear to be negative because of failure to recognize the disorder in family members, early death of the parent before the onset of symptoms, or late onset of the disease in the affected parent.

Sibs of a proband

  • The risk to the sibs of the proband depends on the genetic status of the proband's parents.
  • If a parent of the proband is affected and/or has a DCTN1 pathogenic variant, the risk to the sibs is 50%.
  • When the parents are clinically unaffected, the risk to the sibs of a proband appears to be low.
  • The sibs of a proband with clinically unaffected parents are still at increased risk for Perry syndrome because of the possibility of reduced penetrance in a parent.
  • If the pathogenic variant found in the proband cannot be detected in the leukocyte DNA of either parent, the risk to sibs is low, but greater than that of the general population because of the possibility of germline mosaicism.

Offspring of a proband. Each child of an individual with Perry syndrome has a 50% chance of inheriting the DCTN1 pathogenic variant.

Other family members. The risk to other family members depends on the status of the proband's parents: if a parent is affected and/or has a DCTN1 pathogenic variant, his or her family members may be at risk.

Related Genetic Counseling Issues

Testing of at-risk asymptomatic adult relatives of individuals with Perry syndrome is possible after molecular genetic testing has identified the specific DCTN1 pathogenic variant in the family. Such testing should be performed in the context of formal genetic counseling. This testing is not useful in predicting age of onset, severity, type of symptoms, or rate of progression in asymptomatic individuals. Testing of asymptomatic at-risk individuals with nonspecific or equivocal symptoms is predictive testing, not diagnostic testing.

Testing of asymptomatic individuals younger than age 18 years who are at risk for adult-onset disorders for which no treatment exists is not considered appropriate, primarily because it negates the autonomy of the child with no compelling benefit. Further, concern exists regarding the potential unhealthy adverse effects that such information may have on family dynamics, the risk of discrimination and stigmatization in the future, and the anxiety that such information may cause.

It is appropriate to consider testing symptomatic individuals regardless of age in a family with an established diagnosis of Perry syndrome.

For more information, see also the National Society of Genetic Counselors position statement on genetic testing of minors for adult-onset conditions and the American Academy of Pediatrics and American College of Medical Genetics and Genomics policy statement: ethical and policy issues in genetic testing and screening of children.

Considerations in families with an apparent de novo pathogenic variant. When neither parent of a proband with an autosomal dominant condition has the pathogenic variant identified in the proband or clinical evidence of the disorder, the pathogenic variant is likely de novo. However, non-medical explanations including alternate paternity or maternity (e.g., with assisted reproduction) or undisclosed adoption could also be explored.

Family planning

  • The optimal time for determination of genetic risk and discussion of the availability of prenatal/preimplantation genetic testing is before pregnancy.
  • It is appropriate to offer genetic counseling (including discussion of potential risks to offspring and reproductive options) to young adults who are affected or at risk.

DNA banking is the storage of DNA (typically extracted from white blood cells) for possible future use. Because it is likely that testing methodology and our understanding of genes, allelic variants, and diseases will improve in the future, consideration should be given to banking DNA of affected individuals.

Prenatal Testing and Preimplantation Genetic Testing

Once the DCTN1 pathogenic variant has been identified in an affected family member, prenatal testing for a pregnancy at increased risk and preimplantation genetic testing for Perry syndrome are possible.

Differences in perspective may exist among medical professionals and within families regarding the use of prenatal testing. While most centers would consider use of prenatal testing to be a personal decision, discussion of these issues may be helpful.


GeneReviews staff has selected the following disease-specific and/or umbrella support organizations and/or registries for the benefit of individuals with this disorder and their families. GeneReviews is not responsible for the information provided by other organizations. For information on selection criteria, click here.

  • American Parkinson Disease Association (APDA)
    135 Parkinson Avenue
    Staten Island NY 10305
    Phone: 800-223-2732 (toll-free); 718-981-8001
    Fax: 718-981-4399
  • Michael J. Fox Foundation for Parkinson's Research
    Church Street Station
    PO Box 780
    New York NY 10008-0780
    Phone: 800-708-7644 (toll-free)
  • National Library of Medicine Genetics Home Reference
  • Parkinson's Foundation
    200 SE 1st Street
    Suite 800
    Miami FL 33131
    Phone: 800-4PD-INFO (473-4636)

Molecular Genetics

Information in the Molecular Genetics and OMIM tables may differ from that elsewhere in the GeneReview: tables may contain more recent information. —ED.

Table A.

Perry Syndrome: Genes and Databases

Data are compiled from the following standard references: gene from HGNC; chromosome locus from OMIM; protein from UniProt. For a description of databases (Locus Specific, HGMD, ClinVar) to which links are provided, click here.

Table B.

OMIM Entries for Perry Syndrome (View All in OMIM)


Molecular Pathogenesis

DCTN1 encodes p150(glued), the major subunit of the dynactin protein complex [Farrer et al 2009]. The dynactin protein complex plays a major role in retrograde axonal and cytoplasmic transport of vesicles, organelles, and other cargos through binding to its complex structure. p150(glued) contains the cytoskeleton-associated protein glycine-rich (CAP-Gly) domain that is essential for microtubule binding. All DCTN1 variants found in individuals with Perry syndrome are located in this domain. In vitro, DCTN1 variants alter the ability of dynactin to bind microtubules, thereby impairing its function as a transport protein [Puls et al 2003, Levy et al 2006, Farrer et al 2009, Lloyd et al 2012, Moughamian & Holzbaur 2012].

The link between DCTN1 pathogenic variants and neuronal dysfunction/death remains to be elucidated. For example, the fact that pathogenic variants causing Perry syndrome and HMN7B are located close to each other yet cause completely different clinical features with distinct distribution of affected neuronal systems constitutes a challenging puzzle [Wider et al 2010].

Gene structure. Alternative splicing of this gene results in multiple transcript variants encoding distinct isoforms. The reference sequence NM_004082.3 is known as isoform 1; details of other isoforms are available at Entrez Gene.

Pathogenic variants. All reported Perry syndrome-associated pathogenic variants in DCTN1 are missense variants. These variants induce a loss of CAP-Gly function. The p.Gly71Arg variant has a dominant-negative effect on initiation of retrograde transport [Moughamian & Holzbaur 2012].

Table 2.

DCTN1 Selected Pathogenic Variants

DNA Nucleotide ChangePredicted Protein ChangeReference Sequences
c.167A>Gp.Lys56Arg 1
c.175G>Ap.Gly59Ser 2

Variants listed in the table have been provided by the authors. GeneReviews staff have not independently verified the classification of variants.

GeneReviews follows the standard naming conventions of the Human Genome Variation Society (varnomen​ See Quick Reference for an explanation of nomenclature.


This pathogenic variant has been identified in individuals with clinical PSP (no autopsy confirmation).


This pathogenic variant causes HMN7B.

Normal gene product. DCTN1 encodes p150(glued), the major subunit of the dynactin protein complex, which plays an important role in axonal and cytoplasmic transport.

Abnormal gene product. DCTN1 harboring single-nucleotide variants that cause Perry syndrome and HMN7B encodes abnormal forms of p150(glued), which alter the affinity of dynactin for microtubules. Pathogenic variants associated with Perry syndrome are exposed to the surface of the CAP-Gly domain of p150(glued) [Moughamian & Holzbaur 2012]. This abnormal p150(glued) fails to accumulate dynactin at the neurite tip, resulting in disruption of retrograde flux [Moughamian & Holzbaur 2012].


Literature Cited

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Chapter Notes


Dr Wszolek is supported by NIH/NINDS P50NS072187, NIH/NIA (primary) and NIH/NINDS (secondary) 1U01AG045390-01A1, Mayo Center for Regenerative Medicine, Mayo Clinic Neuroscience Focused Research Team (Cecilia and Dan Carmichael Family Foundation, and the James C and Sarah K Kennedy Fund for Neurodegenerative Disease Research at Mayo Clinic in Florida), and The Sol Goldman Charitable Trust.

Dr Konno is supported by the JSPS Postdoctoral Fellowship for Research Abroad, and the gift from Carl Edward Bolch, Jr and Susan Bass Bolch.

Author History

Takuya Konno, MD (2016-present)
Christian Wider, MD; Centre Hospitalier Universitaire Vaudois, Lausanne (2010-2016)
Zbigneiw Wszolek, MD (2010-present)

Revision History

  • 29 September 2016 (sw) Comprehensive update posted live
  • 9 May 2013 (me) Comprehensive update posted live
  • 30 September 2010 (me) Review posted live
  • 3 May 2010 (cw) Original submission
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