Neurodegeneration in the age of molecular biology

British Medical Journal

Volumn 324, Issue 7352, 2002, Pages 1467-1468

  Golbe, Lawrence I ^a  

^a ROBERT WOOD JOHNSON MEDICAL SCHOOL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ALPHA SYNUCLEIN; TAU PROTEIN;

CELL FUNCTION; EDITORIAL; ENVIRONMENTAL EXPOSURE; HUMAN; LEWY BODY; MOLECULAR BIOLOGY; NERVE DEGENERATION; OLIGODENDROGLIA; OLIVOPONTOCEREBELLAR ATROPHY; OXIDATIVE STRESS; PATHOGENESIS; PRIORITY JOURNAL; PROTEIN AGGREGATION; PROTEIN FOLDING; PROTEIN STRUCTURE; RISK ASSESSMENT; RISK FACTOR;

EID: 0037157540     PISSN: 09598146     EISSN: None     Source Type: Journal    
DOI: 10.1136/bmj.324.7352.1467     Document Type: Editorial

References (13)

1. The tau A0 allele in Parkinson's disease
2. Alpha-synuclein in Lewy bodies
3. Vesicle permeabilization by protofibrillar α-synuclein is sensitive to Parkinson's disease-linked mutations and occurs by a pore-like mechanism
4. Kinetic stabilization of the synuclein protofibril by a dopamine-synuclein adduct
5. Inherent toxicity of aggregates implies a common mechanism for protein misfolding diseases
6. Impairment of the ubiquitin-proteasome system by protein aggregation
7. Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism
8. A large kindred with autosomal dominant Parkinson's disease
9. Mutation in alpha-synuclein identified in families with Parkinson's disease
10. Chronic systemic pesticide exposure reproduces features of Parkinson's disease
11. Metal-triggered structural transformations, aggregation, and fibrillation of human alpha-synuclein. A possible molecular link between Parkinson's disease and heavy metal exposure
12. Oxidative stress induces amyloid-like aggregate formation of NACP/alpha-synuclein in vitro
13. Widespread alterations in alpha-synuclein in multiple system atrophy