In the study, β-amyloid plaque density and synaptophysin immunoreactivity in the brains of the rhesus monkeys that had lived in standard sized cages VS small cages (29% smaller than standard cages) for the first 15 years were compared. Young monkeys were also used as a basis for comparison.
β-amyloid plaque density
β-amyloid deposition has been established as the central cause of Alzheimer’s disease (Hardy & Allsop, 1991). The researchers found that monkeys that were housed in small cages had higher β-amyloid plaque density and amyloid load in the superior temporal gyrus compared to monkeys that were housed in standard sized cages. Young monkeys had no detectable amyloid deposition and were not graphed.
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However, I think the β-amyloid density results should be taken with a pinch of salt. Although the authors did mention that there is considerable individual variation - which parallels data in human studies, the effects seemed to be heavily driven by the monkey which had almost 140 plaques per mm square. Also, there were only 5 monkeys in the small cage condition and 3 of them appear to have comparable β-amyloid density levels. The authors also did not include individual data for the superior temporal gyrus amyloid load graph but the large error bar again suggests significant individual variations.
Monkeys reared in small cages also showed a reduction in synaptophysin immunoreactivity - a presynaptic marker, in the superior temporal gyrus. This indicates a decrease in synaptic density and activity which has been linked with cognitive impairment in Alzheimer's disease.
Merrill DA, Masliah E, Roberts JA, McKay H, Kordower JH, Mufson EJ, & Tuszynski MH (2011). Association of early experience with neurodegeneration in aged primates. Neurobiology of aging, 32 (1), 151-6 PMID: 19321231