IC-PL-01: Aging of the brain: Neurobiology and imaging

Abstract

To comprehend causes and mechanisms of age–related degenerative brain disease we need to understand the course of the normal and successful aging. Summarize neuroimaging findings pertaining to normal brain aging. Narrative and quantitative review of the literature. In vivo cross–sectional studies suggest differential brain aging with the prefrontal cortex more affected than the rest of the neocortex. Smaller age differences are observed in temporal, parietal and occipital cortices. The volumes of the hippocampus, amygdala, striatum and cerebellum show moderately negative association with age; the entorhinal cortex shows little age–related differences. The white matter volume increases throughout development, remains stable in the middle–aged, and is reduced in the older people. White matter integrity indices (white matter hyperintensities, WMH; fractional anisotropy, FA) are compromised only in older individuals, especially in the anterior regions. Longitudinal studies confirm the notion of differential aging. Association cortices (prefrontal, parietal, and temporal) tend to shrink faster than the sensory regions (primary visual). However, the neostriatum and the cerebellum exhibit as significant a change as the association cortices. The shrinkage of the hippocampus is minimal in the middle age but accelerates during the later part of the lifespan. Entorhinal cortex maintains stable volume during most of adulthood but begins to shrink significantly in the sixth decade of life. Shrinkage rates and increase in WMH burden in some regions depend on age–associated pathological factors (vascular risk and vascular disease). The prefrontal cortices, the hippocampus and the white matter are vulnerable to such negative modifiers. However, the prefrontal cortices and the white matter may be responsive to positive modifying intervention such as aerobic exercise. Although cognitive performance is differentially compromised in older adults, the magnitude of declines may depend on differential shrinkage of specific brain regions (e.g. entorhinal) and presence of vascular risk factors. Although brain exhibits regional shrinkage even in successful aging, its magnitude and relation to cognition are affected by concomitant subclinical pathology, which can be prevented, delayed or modified.