β-Amyloid peptides enhance α-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer's disease and Parkinson's disease

Proceedings of the National Academy of Sciences of the United States of America

Volumn 98, Issue 21, 2001, Pages 12245-12250

  Masliah, Eliezer ^a,b   Rockenstein, Edward ^a   Veinbergs, Isaac ^b   Sagara, Yutaka ^a   Mallory, Margaret ^a   Hashimoto, Makoto ^a   Mucke, Lennart ^c  

^a UNIVERSITY OF CALIFORNIA   (United States)

^b UNIVERSITY OF CALIFORNIA   (United States)

^c UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ALPHA SYNUCLEIN; AMYLOID BETA PROTEIN;

ADOLESCENT; AGED; AGING; ALZHEIMER DISEASE; AMNESIA; ANIMAL CELL; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL CULTURE; CELL FREE SYSTEM; CELL INCLUSION; CELL ULTRASTRUCTURE; CHOLINERGIC NERVE CELL; CONTROLLED STUDY; DIFFUSE LEWY BODY DISEASE; GENE EXPRESSION; LEARNING DISORDER; MOUSE; NERVE CELL DEGENERATION; NONHUMAN; NUCLEOTIDE SEQUENCE; PARKINSON DISEASE; PRESYNAPTIC NERVE; PRIORITY JOURNAL; TRANSGENIC MOUSE;

AGE FACTORS; ALPHA-SYNUCLEIN; ALZHEIMER DISEASE; AMYLOID BETA-PROTEIN; ANIMALS; CELL LINE; DISEASE MODELS, ANIMAL; FEMALE; GENE EXPRESSION; HUMANS; LEARNING DISORDERS; MALE; MEMORY DISORDERS; MICE; MICE, TRANSGENIC; NERVE TISSUE PROTEINS; NEURONS; PARKINSON DISEASE; SYNUCLEINS;

EID: 0035834076     PISSN: 00278424     EISSN: None     Source Type: Journal    
DOI: 10.1073/pnas.211412398     Document Type: Article

References (54)