Our monkeys are aging. As they do, we notice decline in noticing things, remembering things, and ability to move. There have been a few cases that appear to have Parkinson’s Disease, and most die of causes typical of humans as well (cancer, cardiovascular issues, stroke).
Quince, our oldest monkey, at 24 years of age, a few months before she passed away of natural causes. We miss her!
Cotton-top tamarins display age-dependent beta-amyloid (Aβ) pathology in cortical layers and display cerebral amyloid angiopathy (Lemere et al., 2008). Specifically, tamarins 12 years of age or older at death showed Aβ in blood vessels, and by 13 years, in plaques, as evidenced in this seminal research by Lemere.
The broad objective of our current research is to test our tamarins, a primate model that already shows evidence of Aβ plaque accumulation, to determine whether there are cognitive and behavioral deficits that correlate with plaque accumulation. We also look for hyperphosphorylated tau accumulation, increased reactive or dystrophic astrocytes and microglia accumulation, and loss of neural cells after our monkeys pass on. A central question is whether their cognitive deficits measured in life and physiological changes measured post-mortem are ones also found in Alzheimer’s Disease (AD) in humans. Cognitive tasks that show a unique decline in human patients include immediate forgetting, category set shifting failures, and visuospatial search failures. A matching-to-sample task, a traditional memory task for animals, is employed to test forgetting over short periods of time of various sets of objects. A visual search task in which targets are provided in one of 4 quadrants tests visuospatial search slowness or failures. A dimensional change card sorting (DCCS) task commonly used to test toddlers who also fail to shift sets is used to measure resistance to shift rules in the primate model.
Individual differences in cognitive decline and in vital behaviors (foraging, social, motor) are tracked over time and used in a multiple regression analysis to determine the best predictor of physiological decline (Aβ plaque accumulation, tau accumulation, immune response activation, and neural degeneration) from the cognitive signature provided in life. Immunohistochemical assessment in brain tissue will verify the presence of Aβ plaques, tau, microglia, astrocytes, and cells. If successful, the cognitive, behavioral and physiological methods will elucidate aging and neurodegenerative disease expression in tamarins. Finding a good set of tasks to evaluate primates could lead to new medical and training procedures and may elucidate specific relationships between AD markers, immune response, and cognitive limits that could move us closer to treatments to stop or arrest AD-like processes and other limitations brought on with age.