Carlo Bertoni-Freddari, Patrizia Fattoretti, Tiziana Casoli, and Giuseppina Di Stefano
Different anatomical, histological, cellular, and sub-cellular alterations occur in the human brain during aging. Because of this wide variety of changes, often masked by compensating reactions, the identification of clear-cut decays due to age may constitute a difficult task. In the elderly, brain volume and weight decrease because of an insignificant loss of neurons, dendritic atrophy, and glial cells degeneration. Damage of blood vessels, due to atherosclerosis and amyloid angiopathy, by reducing brain blood perfusion, may play a role in neuronal, glial, and dendritic degenerative phenomena. Impaired cellular membrane turnover leads to accumulation of age pigments or lipofuscin. Loss of synapses, paired with an imbalance of neurotransmitter systems, occurs in physiological and, to a higher degree, pathological aging.
Brain energy metabolism also declines in aging, which involves a decay in the mitochondrial metabolic competence that can be considered an unfavorable condition affecting several other processes such as calcium home-ostasis and the development of SP and NFT. Nonhuman primates and transgenic mice, presently adopted as animal models to investigate human brain aging and AD, may further our understanding of the mechanisms underlying the formation of Alzheimer-like alterations, and may help to set up intervention strategies leading to an increase of the percent of cognitive intact and successfully aged subjects.
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