Cerebrospinal fluid lysosomal enzymes and alpha‐synuclein in Parkinson's disease-Reference-Cited by-同舟云学术

Cerebrospinal fluid lysosomal enzymes and alpha‐synuclein in Parkinson's disease

Published:2014-01-16 Issue:8 Volume:29 Page:1019-1027
ISSN:0885-3185
Container-title:Movement Disorders
language:en
Short-container-title:Mov Disord.

Author:

Parnetti Lucilla¹,Chiasserini Davide¹²,Persichetti Emanuele³,Eusebi Paolo⁴,Varghese Shiji⁵,Qureshi Mohammad M.⁵,Dardis Andrea⁶,Deganuto Marta⁶,Carlo Claudia¹,Castrioto Anna¹,Balducci Chiara³,Paciotti Silvia³,Tambasco Nicola¹,Bembi Bruno⁶,Bonanni Laura⁷,Onofrj Marco⁷,Rossi Aroldo¹,Beccari Tommaso³,El‐Agnaf Omar⁵⁸,Calabresi Paolo¹²

Affiliation:

1. Clinica NeurologicaUniversità degli Studi di PerugiaPerugia Italy

2. Fondazione S. LuciaL'Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS)Rome Italy

3. Department of Economic Sciences and Food Sciences (DSEEA)Section of Food Chemistry, Biochemistry, Physiology and Nutrition, University of PerugiaPerugia Italy

4. Department of EpidemiologyRegional Health Authority of UmbriaPerugia Italy

5. Department of Biochemistry Faculty of Medicine and Health SciencesUnited Arab Emirates UniversityAl Ain United Arab Emirates

6. Regional Coordinating Centre for Rare DiseasesUniversity Hospital “Santa Maria della Misericordia,”Udine Italy

7. Department of Neuroscience and ImagingUniversity G. D'Annunzio of Chieti‐PescaraChieti Italy

8. Faculty of MedicineKing Abdulaziz UniversityJeddah Saudi Arabia

Publisher

Wiley

Subject

Neurology (clinical),Neurology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/mds.25772

Reference45 articles.

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2. Acceleration of oligomerization, not fibrillization, is a shared property of both alpha -synuclein mutations linked to early-onset Parkinson's disease: Implications for pathogenesis and therapy

3. Pre-fibrillar α-synuclein variants with impaired β-structure increase neurotoxicity in Parkinson's disease models

4. In vivo demonstration that -synuclein oligomers are toxic

5. Clinical and pathological features of a parkinsonian syndrome in a family with an Ala53Thr ?-synuclein mutation

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