Table 4.

AD-related pathologic and inflammatory traits observed in chimpanzees and humans.

DIVERGENT TRAITS		SHARED TRAITS
Chimpanzee	Human	Chimpanzee + Human
Deposition of Aβ is primarily in the brain’s vessels and occurs prior to formation of plaques.	Deposition of Aβ is primarily in the form of plaques, although CAA occurs in most AD patients.	Aβ pathology increases with age.
Aβ42 is the predominant peptide in severe CAA.	Aβ40 is the primary protein in humans with severe CAA.	Aβ pathology is associated with increased tau pathology.
Tau neuritic clusters lack an Aβ core.	Neuritic plaques contain an Aβ core.	Tau deposition occurs in microglia.
Pretangles in the neocortex increase with age.	NFT increase with age in the hippocampus.	NFT density is higher in hippocampal subfield CA1 compared to CA3.
Activated microglia density is higher in CA3 compared to CA1.	AD patients had higher microglial activation in CA1, despite control groups presenting with greater microglia density in the CA3.	Severe CAA is associated with increased tau pathology (NFT in humans; pretangles and tau neuritic clusters in chimpanzees).
Microglial activation is correlated with Aβ but not NFT lesions.	Microglial activation is associated with Aβ and NFT pathology.	Aβ42 is correlated with increased microglial activation (plaques in humans, vessels in chimpanzees).
Neuron loss in association with AD pathology has not yet been quantified in chimpanzees.	Selective neuronal loss occurs in the prefrontal cortex and hippocampus.
Antemortem cognitive testing is rare in aged apes. Mild cognitive deficits in short-term and spatial memory, attention, and executive function have been noted.	Severe memory, cognitive, and behavioral deficits are observed.