Attention conservation notice: This is an important but hotly debated question and I’m not nearly well-versed enough in the field to provide an answer. Instead, I’ll summarize a 2012 review and a little bit of external data in table format.
Why does this matter? Well, if some non-human primates get Alzheimers dementia and others don’t, or, even better, if there were a spectrum of Alzheimers pathology and clinical symptoms among NHPs, then this could be correlated with genomic or transcriptomic data to get a better sense of the mechanism of the disease.
According to this 2012 review by Heuer et al, there are two major areas where research has been done across NHP species: histological and behavioral.
Histologically, the major areas are:
- The presence of amyloid plaques (+/- soluble oligomers) that show up at ~ 80% (+/-, say, 20%) of the species’s maximum lifespan
- The presence of abnormally phosphorylated tau
- The presence of cerebral amyloid angiopathy
- The presence of substantial neuron loss
Behaviorally, the major areas are:
- Executive deficits
- Memory deficits
This google spreadsheet summarizes the type of pathology present for each of the above, for each type of NHP species, where available.
A summary of the data is that great apes (i.e., the NHPs closest to humans) have executive but not memory deficits in aging, the latter of which is consistent with them having amyloid plaques but no major neuron loss.
If you have any suggestions, please make comments on the spreadsheet and I’ll incorporate them.
Heuer E, Rosen RF, Cintron A, Walker LC. Nonhuman primate models of Alzheimer-like cerebral proteopathy. Curr Pharm Des. 2012;18(8):1159-69.
Erwin J, Hof PR. Aging in Nonhuman Primates. Karger Medical and Scientific Publishers; 2002.
Darusman HS, Pandelaki J, Mulyadi R, et al. Poor memory performance in aged cynomolgus monkeys with hippocampal atrophy, depletion of amyloid beta 1-42 and accumulation of tau proteins in cerebrospinal fluid. In Vivo. 2014;28(2):173-84.