beta-amyloid is different in normal aging and in Alzheimer disease.
The mechanism of neurodegeneration caused by beta-amyloid in Alzheimer disease is controversial. Neuronal toxicity is exerted mostly by various species of soluble beta-amyloid oligomers that differ in their N- and C-terminal domains. However, abundant accumulation of beta-amyloid also occurs in the brains of cognitively normal elderly people, in the absence of obvious neuronal dysfunction. We postulated that neuronal toxicity depends on the molecular composition, rather than the amount, of the soluble beta-amyloid oligomers. Here we show that soluble beta-amyloid aggregates that accumulate in Alzheimer disease are different from those of normal aging in regard to the composition as well as the aggregation and toxicity properties.
Piccini
Alessandra
A
Department of Neurosciences, Ophthalmology, and Genetics, University of Genoa, Genoa, Italy.
Russo
Claudio
C
Gliozzi
Alessandra
A
Relini
Annalisa
A
Vitali
Antonella
A
Borghi
Roberta
R
Giliberto
Luca
L
Armirotti
Andrea
A
D'Arrigo
Cristina
C
Bachi
Angela
A
Cattaneo
Angela
A
Canale
Claudio
C
Torrassa
Silvia
S
Saido
Takaomi C
TC
Markesbery
William
W
Gambetti
Pierluigi
P
Tabaton
Massimo
M
D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000378:metabolism*; D000544:Alzheimer Disease / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000032:analysis / Q000737:chemistry*; D016022:Case-Control Studies; D016923:Cell Death; D005260:Female; D006801:Humans; D008297:Male; D009474:Neurons
D016229:Amyloid beta-Peptides