Investigators have wondered why the brains of some cognitively-intact elderly individuals have abundant pathology on autopsy or significant amyloid deposition on neuroimaging that are characteristic of Alzheimer disease (AD). Researchers reporting in The American Journal of Pathology investigated biochemical factors and identified differences in proteins from parietal cortex synapses between patients with and those without manifestation of dementia. Specifically, early-stage AD patients had elevated concentrations of synaptic soluble amyloid-β (Aβ) oligomers compared to controls who were not demented but displayed signs of AD pathology. Synapse-associated hyperphosphorylated tau (p-tau) levels did not increase until late-stage AD.
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