Journal
JOURNAL OF CHEMICAL NEUROANATOMY
Volume 128, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.jchemneu.2022.102210
Keywords
Aging; Antioxidants; Cell senescence; Mitochondria; Reactive oxygen species
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Aging is a natural process characterized by the accumulation of cellular damage and debris. It is associated with oxidative stress, cellular senescence, sustained inflammation, and DNA damage, leading to morphological and functional decline. The atrophy is mainly observed in high metabolic tissues such as the brain, particularly in regions related to cognitive behavior. This article reviews the cellular processes triggering aging, distinguishes between normal and pathological aging, and discusses the use of supplements with antioxidant and anti-inflammatory properties in reducing cognitive decline.
Aging is a natural phenomenon characterized by accumulation of cellular damage and debris. Oxidative stress, cellular senescence, sustained inflammation, and DNA damage are the main cellular processes characteristic of aging associated with morphological and functional decline. These effects tend to be more pronounced in tissues with high metabolic rates such as the brain, mainly in regions such as the prefrontal cortex, hippocampus, and amygdala. These regions are highly related to cognitive behavior, and therefore their atrophy usually leads to decline in processes such as memory and learning. These cognitive declines can occur in physiological aging and are exacerbated in pathological aging. In this article, we review the cellular processes that underlie the triggers of aging and how they relate to one another, causing the atrophy of nerve tissue that is typical of aging. The main topic of this review to determine the central factor that triggers all the cellular processes that lead to cellular aging and discriminate between normal and pathological aging. Finally, we review how the use of supplements with antioxidant and anti-inflammatory properties reduces the cognitive decline typical of aging, which re-inforces the hypothesis of oxidative stress and cellular damage as contributors of physiological atrophy of aging. Moreover, cumulative evidence suggests their possible use as therapies, which improve the aging population's quality of life.
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