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Items: 1 to 20 of 110

1.

PET and MRI reveal early evidence of neurodegeneration in spinocerebellar ataxia type 17.

Brockmann K, Reimold M, Globas C, Hauser TK, Walter U, Machulla HJ, Rolfs A, Schöls L.

J Nucl Med. 2012 Jul;53(7):1074-80. doi: 10.2967/jnumed.111.101543.

2.

Importance of low-range CAG expansion and CAA interruption in SCA2 Parkinsonism.

Kim JM, Hong S, Kim GP, Choi YJ, Kim YK, Park SS, Kim SE, Jeon BS.

Arch Neurol. 2007 Oct;64(10):1510-8.

PMID:
17923635
3.

No parkinsonism in SCA2 and SCA3 despite severe neurodegeneration of the dopaminergic substantia nigra.

Schöls L, Reimold M, Seidel K, Globas C, Brockmann K, Hauser TK, Auburger G, Bürk K, den Dunnen W, Reischl G, Korf HW, Brunt ER, Rüb U.

Brain. 2015 Nov;138(Pt 11):3316-26. doi: 10.1093/brain/awv255.

PMID:
26362908
4.

Structural changes associated with progression of motor deficits in spinocerebellar ataxia 17.

Reetz K, Lencer R, Hagenah JM, Gaser C, Tadic V, Walter U, Wolters A, Steinlechner S, Zühlke C, Brockmann K, Klein C, Rolfs A, Binkofski F.

Cerebellum. 2010 Jun;9(2):210-7. doi: 10.1007/s12311-009-0150-4.

PMID:
20016963
5.

Biological and clinical characteristics of individuals at risk for spinocerebellar ataxia types 1, 2, 3, and 6 in the longitudinal RISCA study: analysis of baseline data.

Jacobi H, Reetz K, du Montcel ST, Bauer P, Mariotti C, Nanetti L, Rakowicz M, Sulek A, Durr A, Charles P, Filla A, Antenora A, Schöls L, Schicks J, Infante J, Kang JS, Timmann D, Di Fabio R, Masciullo M, Baliko L, Melegh B, Boesch S, Bürk K, Peltz A, Schulz JB, Dufaure-Garé I, Klockgether T.

Lancet Neurol. 2013 Jul;12(7):650-8. doi: 10.1016/S1474-4422(13)70104-2. Erratum in: Lancet Neurol. 2013 Jul;12(7):630.

PMID:
23707147
6.

Morphological basis for the spectrum of clinical deficits in spinocerebellar ataxia 17 (SCA17).

Lasek K, Lencer R, Gaser C, Hagenah J, Walter U, Wolters A, Kock N, Steinlechner S, Nagel M, Zühlke C, Nitschke MF, Brockmann K, Klein C, Rolfs A, Binkofski F.

Brain. 2006 Sep;129(Pt 9):2341-52.

PMID:
16760196
7.

Functional brain imaging in glucocerebrosidase mutation carriers with and without parkinsonism.

Kono S, Ouchi Y, Terada T, Ida H, Suzuki M, Miyajima H.

Mov Disord. 2010 Sep 15;25(12):1823-9. doi: 10.1002/mds.23213.

PMID:
20669267
8.

Dopamine transporter positron emission tomography in spinocerebellar ataxias type 1, 2, 3, and 6.

Wüllner U, Reimold M, Abele M, Bürk K, Minnerop M, Dohmen BM, Machulla HJ, Bares R, Klockgether T.

Arch Neurol. 2005 Aug;62(8):1280-5.

PMID:
16087769
9.

Striatal glucose metabolism and dopamine D2 receptor binding in asymptomatic gene carriers and patients with Huntington's disease.

Antonini A, Leenders KL, Spiegel R, Meier D, Vontobel P, Weigell-Weber M, Sanchez-Pernaute R, de Yébenez JG, Boesiger P, Weindl A, Maguire RP.

Brain. 1996 Dec;119 ( Pt 6):2085-95.

PMID:
9010012
10.

The SCA17 phenotype can include features of MSA-C, PSP and cognitive impairment.

Lin IS, Wu RM, Lee-Chen GJ, Shan DE, Gwinn-Hardy K.

Parkinsonism Relat Disord. 2007 May;13(4):246-9.

PMID:
16793320
11.

Brain white-matter volume loss and glucose hypometabolism precede the clinical symptoms of Huntington's disease.

Ciarmiello A, Cannella M, Lastoria S, Simonelli M, Frati L, Rubinsztein DC, Squitieri F.

J Nucl Med. 2006 Feb;47(2):215-22.

12.

Construction and evaluation of multitracer small-animal PET probabilistic atlases for voxel-based functional mapping of the rat brain.

Casteels C, Vermaelen P, Nuyts J, Van Der Linden A, Baekelandt V, Mortelmans L, Bormans G, Van Laere K.

J Nucl Med. 2006 Nov;47(11):1858-66.

13.

Genotype-specific patterns of atrophy progression are more sensitive than clinical decline in SCA1, SCA3 and SCA6.

Reetz K, Costa AS, Mirzazade S, Lehmann A, Juzek A, Rakowicz M, Boguslawska R, Schöls L, Linnemann C, Mariotti C, Grisoli M, Dürr A, van de Warrenburg BP, Timmann D, Pandolfo M, Bauer P, Jacobi H, Hauser TK, Klockgether T, Schulz JB; axia Study Group Investigators..

Brain. 2013 Mar;136(Pt 3):905-17. doi: 10.1093/brain/aws369.

PMID:
23423669
14.

A novel transgenic rat model for spinocerebellar ataxia type 17 recapitulates neuropathological changes and supplies in vivo imaging biomarkers.

Kelp A, Koeppen AH, Petrasch-Parwez E, Calaminus C, Bauer C, Portal E, Yu-Taeger L, Pichler B, Bauer P, Riess O, Nguyen HP.

J Neurosci. 2013 May 22;33(21):9068-81. doi: 10.1523/JNEUROSCI.5622-12.2013.

15.

Cerebellum-specific 18F-FDG PET analysis for the detection of subregional glucose metabolism changes in spinocerebellar ataxia.

Oh JS, Oh M, Chung SJ, Kim JS.

Neuroreport. 2014 Oct 22;25(15):1198-202. doi: 10.1097/WNR.0000000000000247.

PMID:
25144395
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19.

PET in LRRK2 mutations: comparison to sporadic Parkinson's disease and evidence for presymptomatic compensation.

Adams JR, van Netten H, Schulzer M, Mak E, Mckenzie J, Strongosky A, Sossi V, Ruth TJ, Lee CS, Farrer M, Gasser T, Uitti RJ, Calne DB, Wszolek ZK, Stoessl AJ.

Brain. 2005 Dec;128(Pt 12):2777-85.

PMID:
16081470
20.

Familial parkinsonism with synuclein pathology: clinical and PET studies of A30P mutation carriers.

Krüger R, Kuhn W, Leenders KL, Sprengelmeyer R, Müller T, Woitalla D, Portman AT, Maguire RP, Veenma L, Schröder U, Schöls L, Epplen JT, Riess O, Przuntek H.

Neurology. 2001 May 22;56(10):1355-62.

PMID:
11376188

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