The late 1980s through the 1990s produced a shift toward region- and process-specific neural aging. Imaging studies revealed disproportionate age-related loss in prefrontal gray matter, signaling region-specific vulnerability and challenging the notion of uniform cortical decline. Challenging dogma of hippocampal uniform aging, animal models showed preserved hippocampal neuron numbers despite spatial learning deficits, implicating synaptic and circuit changes rather than neuron loss as the basis for functional decline. The aging and inhibition literature demonstrated that older adults exhibit selective impairment across tasks rather than a single inhibitory deficit, steering targeted investigations into heterogeneity of cognitive aging. Pathology studies with transgenic models showed amyloid deposition can accumulate without CA1 neuronal loss, refining interpretations of age-related neuropathology and disease models.