Age-related cerebrovascular pathologies, ranging from cerebromicrovascular functional
and structural alterations to large vessel atherosclerosis, promote the genesis of
vascular cognitive impairment and dementia (VCID) and exacerbate Alzheimer’s disease.
Recent advances in geroscience, including results from studies on heterochronic parabiosis
models, reinforce the hypothesis that cell non-autonomous mechanisms play a key role
in regulating cerebrovascular aging processes. Growth hormone (GH) and insulin-like
growth factor 1 (IGF-1) exert multifaceted vasoprotective effects and production of
both hormones is significantly reduced in aging. This brief overview focuses on the
role of age- related GH/IGF-1 deficiency in the development of cerebrovascular pathologies
and VCID. It explores the mechanistic links among alterations in the somatotropic
axis, specific macrovascular and microvascular pathologies (including capillary rarefaction,
microhemorrhages, impaired endothelial regulation of cerebral blood flow, disruption
of the blood brain barrier, decreased neurovascular coupling, and atherogenesis) and
cognitive impairment. Improved understanding of cell non- autonomous mechanisms of
vascular aging is crucial to identify targets for intervention to promote cerebrovascular
and brain health in older adults.
