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Cerebral amyloid beta(42) deposits and microvascular pathology in ageing baboons

Lookup NU author(s): Michael Ndung'U, Dr Rufus Akinyemi, Professor Raj KalariaORCiD

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Abstract

M. Ndung'u, W. Hartig, F. Wegner, J. M. Mwenda, R. W. C. Low, R. O. Akinyemi and R. N. Kalaria (2012) Neuropathology and Applied Neurobiology38, 487-499 Cerebral amyloid beta(42) deposits and microvascular pathology in ageing baboons Background: Previous studies have extensively reported the deposition of amyloid beta (A beta) peptide with carboxyl- and amino-terminal heterogeneity in cortical and cerebrovascular deposits in Alzheimer's disease (AD) and in non-human primates except baboons. Methods: We examined the immunocytochemical distribution of A beta peptides and A beta oligomers in brain tissue from three subspecies of 18- to 28-year-old baboons (Papio) and in other monkeys including the squirrel (Saimiri sciureus) and rhesus (Macaca mulatta) for comparison. Results: A general preponderance of A beta(42) in parenchymal deposits and many vascular deposits in all cortical lobes was evident in the baboons. A beta oligomeric immunoreactivity was also apparent like to amyloid plaques. We found that the amino acid sequence of the A beta domain of the baboon amyloid precursor protein is similar to that of man. In contrast to A beta, immunoreactivity to hyperphosphorylated tau protein was largely intracellular and rare in these baboons. Brain tissues from squirrel and rhesus monkeys examined in parallel exhibited mostly vascular and parenchymal deposits containing A beta(42) peptides. Our results were comparable to AD, but showed that even in younger monkeys exhibiting few deposits, A beta(42) was evident in both parenchymal deposits and cerebral amyloid angiopathy. Perivascular amyloid deposits were frequent and often accompanied by microvascular abnormalities in the form of collapsed degenerated capillaries. Conclusions: Similar to other primates above and below in the phylogenetic order, our observations and evaluation of the literature implicate pathogenicity of A beta(42) peptide associated with microvascular degeneration in baboons. We suggest baboons are useful animals to investigate the dynamics of AD-related pathology.


Publication metadata

Author(s): Ndung'u M, Hartig W, Wegner F, Mwenda JM, Low RWC, Akinyemi RO, Kalaria RN

Publication type: Article

Publication status: Published

Journal: Neuropathology and Applied Neurobiology

Year: 2012

Volume: 38

Issue: 5

Pages: 487-499

Print publication date: 06/07/2012

ISSN (print): 0305-1846

ISSN (electronic): 1365-2990

Publisher: Wiley-Blackwell Publishing Ltd.

URL: http://dx.doi.org/10.1111/j.1365-2990.2011.01246.x

DOI: 10.1111/j.1365-2990.2011.01246.x


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Funding

Funder referenceFunder name
Medical Research Council
Alzheimer Research Trust, UK
AG10003National Institutes of Health (NINDS)

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