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.

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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.