Gene-environment interactions (GxE) can have lasting consequences on brain structure
and function, potentially contributing to diverse neuropsychiatric phenotypes. This has been extensively
demonstrated by studies examining GxE in childhood and early adulthood, whereas much
fewer studies have addressed this question in late life. The relative paucity of studies examining
GxE in late life may stem from the working hypothesis that brains become less malleable to environmental
inputs as life progresses. However, while some components of brain plasticity decline
with increasing age, others are retained and may even become more pronounced in old ages.
Moreover, the micro- and macro-structural brain changes that accrue as a result of aging-related
morbidities are likely to accentuate the susceptibility of neural circuits to environmental stressors as
life advances. Supporting this hypothesis, psychosocial stress can increase the risk for late-life neuropsychiatric
syndromes, especially when afflicting genetically predisposed individuals. This article
reviews evidence showing how gene-stress interactions can impact the aging brain and related phenotypes
in late life, and it discusses the potential mechanisms underlying such GxE and their implications
for the prevention and treatment of late-life neuropsychiatric syndromes.
Keywords: Aging, BDNF, dementia, gene-environment interactions, late-life depression, neuropsychiatric disorders, neuroscience,
psychosocial stress, serotonin transporter.
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