Very long term studies of the seeding of beta-amyloidosis in primates

• Published in: Journal of Neural Transmission Vol. 113; no. 9; pp. 1243 - 1251
• Main Authors: Ridley, R M, Baker, H F, Windle, C P, Cummings, R M
• Format: Journal Article
• Language: English
• Published: Austria 01.09.2006
• Subjects: Adult; Aging - metabolism; Aging - pathology; Amyloid beta-Peptides - cerebrospinal fluid; Amyloid beta-Peptides - metabolism; Amyloid beta-Peptides - toxicity; Amyloidosis - chemically induced; Amyloidosis - metabolism; Amyloidosis - pathology; Animals; Brain - metabolism; Brain - pathology; Brain - physiology; Callithrix; Down Syndrome - metabolism; Female; Gerstmann-Straussler-Scheinker Disease - metabolism; Humans; Male; Middle Aged; Peptide Fragments - toxicity; Primates
• ISSN: 0300-9564; 1435-1463
• DOI: 10.1007/s00702-005-0385-2

Cerebral beta-amyloidosis was found in 16/18 marmosets aged <10 yrs and 8/9 marmosets aged >10 yrs, injected intracerebrally with human or marmoset brain homogenate containing beta-amyloid 1-8 years previously. It was found in only 2/12 marmosets aged <10 yrs and 1/15 marmosets aged >10 yrs, injected with synthetic Abeta-peptides, CSF, or brain tissue which did not contain beta-amyloid. Cerebral beta-amyloidosis was found in 0/11 uninjected marmosets aged <10 yrs and in 5/29 uninjected marmosets aged >10 yrs. The beta-amyloidosis comprised small and large vessel angiopathy and some plaques throughout cortex and was qualitatively similar in injected marmosets and, when present, in uninjected marmosets. Of those injected marmosets which were positive, the amount of beta-amyloidosis was unrelated to age or incubation times but the 3 injected marmosets without beta-amyloidosis had incubation times of <3.5 years. We conclude that beta-amyloid, or associated factors, can initiate or accelerate the process of cerebral amyloidosis in primates.