Evidence for the accumulation of Abeta immunoreactive material in the human brain and in transgenic animal models.
In this review we highlight the evidence for an intracellular origin of Abeta (Aβ) amyloid peptides as well as the observations for a pathological accumulation of these peptides in Alzheimer's disease and Down syndrome, as well as in transgenic animal models. We deliberate on the controversy as to whether the intracellular Aβ immunoreactive material is simply an accumulation of unprocessed full length amyloid precursor protein (APP) or a mix of processed APP fragments including Aβ. Finally, we discuss the possible pathological significance of these intracellular APP fragments and the expected future research directions regarding this thought-provoking problem.
Department of Pharmacology and Therapeutics, McGill University, 3655 Sir William Osler Promenade, Room 1210, Montreal, Quebec, Canada. Claudio.cuello@mcgill.ca
A Claudio
AC
Cuello
Simon
S
Allard
Maria Teresa
MT
Ferretti
D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D030801:Animals, Genetically Modified; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D004314:Down Syndrome / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism*; D051379:Mice; D051381:Rats
D016229:Amyloid beta-Peptides; D047908:Intracellular Signaling Peptides and Proteins