Physical activity (PA) is a well-studied protective factor for

Physical activity (PA) is a well-studied
protective factor for Alzheimer’s disease (AD), with a recent evidence review identifying
it as the modifiable factor with the highest impact on reducing the national
prevalence of AD.1 Several studies have investigated the relationship between
PA, cognition, brain structure, and neuropathological markers of AD among
cognitively normal adults. Available evidence indicates that higher levels of
PA associates with better cognitive performance2 particularly
on measures of visuospatial functioning,3,4 verbal episodic memory,3 and speed and flexibility.4,5 ln a randomized
control trial (RCT) of 58 cognitively middle-aged adults, aerobic exercise training
over a period of six months improved overall cognition, encompassing several
cognitive domains ranging from executive function to processing speed.5

and RCT evidence suggests that engagement in PA is associated with preserved
volume in various brain regions4,6-8
such as the temporal lobe6,7,9,10
and specifically the hippocampal region4,5,8,11,
as well as decreased white matter atrophy.10 Colcombe et al12 reported increased brain volume in older adults who engaged
in aerobic exercise training, but did not see this effect for those randomized
to a stretching and toning condition. Further, PA selectively enhances anterior
hippocampal volume8 and affects volumetric changes in the hippocampus over time,5 though this relationship may differ between men and women.13 Gender differences have similarly been found in cognitive
performance.14 For example, Laurin and colleagues14 found that over a period of
5 years increased levels of PA had a protective effect on cognition in women
but not men.
            In addition
to its effect on brain structure and cognition, PA has been shown to moderate
the effect of age11 and genetic
risk factors,15 such as apolipoprotein
E (APOE) e4 status,16 on AD pathophysiological biomarkers.

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Okonkwo et al11 found an
association between self-reported PA and the attenuation of age-related
alterations in extant AD biomarkers of b-amyloid (Ab) burden, cerebral glucose
metabolism, and hippocampal volume. Interestingly, lower levels of plasma Ab has been observed only among
carriers of the APOE e4 allele
who reported high levels of PA.17 Thus, the
moderating effect of PA may be influenced by level of intensity.9,16-19
Investigators have examined the effect of PA on AD biomarkers through the lens
of meeting activity recommendations established by the Department of Health and
Human Services9 or the American Heart
Association.11,16,18 Meeting these
PA recommendations has been associated with lower Ab burden,16,20 as
measured by cortical binding of the C-Pittsburgh compound B (PiB) tracer in
regions associated with cognitive decline such as the prefrontal cortex and
lateral temporal lobe.18 Moreover, engagement in
moderate intensity PA, but not light or vigorous activity, has been associated
with increased glucose metabolism in select brain regions such as the temporal
gyri, angular gyri, and posterior cingulate.19
            In summary, there is strong
evidence for positive associations between PA and cognitive performance2-4, and PA
and brain volume within AD-relevant structures.5-10 Furthermore,
emerging evidence indicates that PA may also associate with pathophysiological
markers of AD16-20 or modify the
relationship between core AD risk factors (e.g., age and APOE e4 positivity) and biomarker status.11,15