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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. |
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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. |
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