A consistent observation in the aging and cognition
literature is a greater amount of variability in memory
performance with increasing age. This finding is evident
both when age is considered as a cross-sectional
variable and when individual age trajectories are
examined over time; some adults experience great
amounts of cognitive decline while others experience
relatively little. Increased variability suggests that
there are moderators and mediators of cognitive
aging. Two factors in particular, including cerebrovascular
or cardiovascular risk and cognitive reserve,
have received considerable attention as modulators
that may account for some of the increased variability,
and these are potential targets for intervention or
prevention of cognitive decline.
Cerebrovascular or cardiovascular risk factors may
mediate the relationship between chronological age
and the neurobiological changes that underlie cognitive
aging. Increased blood pressure is associated
with reduced psychomotor speed, visuoconstruction
ability, learning, memory, and executive functioning.
Similarly, both insulin resistance and diabetes are
associated with diminished cognitive abilities in later
life. Hyperlipidemia has also been identified as a potential
cerebrovascular risk factor that negatively impacts
cognition in older adults. While it is still somewhat
unclear by what mechanism cerebrovascular or cardiovascular
risk factors impact cognition, it is likely that
they interact with age to have a cumulative effect
on cognition in later life. Furthermore, intervention
studies that target the vascular system, such as cardiovascular
fitness regimens, are associated with increased
cognitive functioning among older adults.
Cognitive reserve is another factor that may
account for the increased variability observed in
cognitive aging. The cognitive reserve hypothesis stems from the observation that there is a disconnection
between degree of brain pathology and its cognitive
manifestation and suggests that the brain actively
attempts to cope with brain pathology by using existing
processing approaches or by recruiting compensatory
networks. Although cognitive reserve is often applied
to clinical entities, such as AD or stroke, it may be
operative among the normal aged. That is, cognitive
reserve may moderate the relationship between
normal age-associated neurobiological changes and
their cognitive outcome. Indeed, proxies for reserve,
such as measures of education or literacy and IQ,
are related to the degree of age-associated memory
decline. Declarative memory scores of older adults
with lower levels of literacy decline at a greater rate
than do those with higher levels of literacy. Like vascular
risk factors, interventions that target cognitive
reserve may improve the course of cognitive aging.
Other factors, such as genes and nutritional exposure,
could potentially impact the course of memory
decline with normal aging. It is also important to
note that the possibility of inclusion of individuals
with insipient dementia may have contaminated
some studies that attempted to elucidate the pattern
of age-associated memory decline, and future studies
of normal aging should focus on disentangling normal
cognitive decline from pathological aging at the earliest
point possible. With the powerful capabilities of neuroimaging
techniques, we can begin to understand the
complex relationships among normal aging, neurobiology,
and cognition while defining potentially modifiable
moderators and mediators of cognitive aging.
See also: Aging of the Brain; Aging of the Brain and
Alzheimer’s Disease; Aging and Memory in Animals;
Basal Forebrain and Memory; Cognition in Aging and
Age-Related Disease; Episodic Memory; Functional
Neuroimaging Studies of Aging; Humans; Lipids and
Membranes in Brain Aging; Metal Accumulation During
Aging; Short Term and Working Memory.