Table 1.

Summary of neuropathologic changes in ageing and Alzheimer's disease in chimpanzees and humans.

pathology	Alzheimer's disease		ageing
	chimpanzee	human	chimpanzee	human
Aβ	Aβ is primarily in blood vessels and occurs prior to plaque formation	Aβ is primarily in plaques, although CAA occurs in 80% of AD patients	chimpanzees demonstrate increased intravascular Aβ deposition with age	humans exhibit increased Aβ deposition in plaques and vessels with age
	Aβ pathology is associated with increased tau pathology
tau	neuritic clusters contain dystrophic tau neurites but lack an Aβ core	neuritic plaques contain an Aβ core	pretangles in the neocortex increase with age	NFT increase with age in the hippocampus
neuro-inflammation	Aβ42 is correlated with increased microglial activation (i.e. plaques in humans, vessels in chimpanzees)		age is not associated with increased microglial or astrocyte density or activation in chimpanzees	humans display both increased microglial activation and density with age
	microglial activation is correlated with Aβ but not NFT lesions	microglial activation is associated with Aβ and NFT pathology
neuron loss	neuron loss occurs in the temporal cortex in association with Aβ deposition in the brain's blood vessels	selective neuronal loss occurs in the prefrontal cortex and hippocampus	neuron loss was observed in the hippocampus of chimpanzees	selective neuronal loss occurs in the subiculum and dentate gyrus but not CA1-CA3 subfields
cognitive impairment	antemortem cognitive testing in chimpanzees with AD pathology has not been performed yet	severe memory, cognitive and behavioural deficits are observed	cognitive testing is rare in aged apes; mild cognitive deficits in spatial memory, attention, executive function, and cognitive flexibility have been noted	processing speed, attention, memory and cognitive flexibility gradually decline during ageing