Prospective clinicopathologic studies show that a large proportion. of
older, nondemented individuals have sufficient numbers of plaques and
tangles to meet neuropathologic criteria for Alzheimer's disease (AD)
. One explanation for this finding is that these individuals had great
er brain reserve, which buffered clinical expression of the disease. T
hree types of brain reserve are discussed: (1) the number of neurons a
nd/or the density of their interconnections in youth, (2) the collecti
on of cognitive strategies for solving problems and taking neuropsycho
logical tests, and (3) the amount of functional brain tissue remaining
at any age. Evidence is presented showing that brain reserve reduces
clinical expression of AD and can be altered through several means, in
cluding early-life nutrition, prevention of cerebrovascular disease an
d intellectual stimulation.