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Physiological Reviews, Vol. 82, No. 3, July 2002, pp. 637-672; 10.1152/physrev.00004.2002.
Copyright ©2002 by the American Physiological Society
Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland
Mattson, Mark P.,
Sic L. Chan, and
Wenzhen Duan.
Modification of Brain Aging and Neurodegenerative Disorders by
Genes, Diet, and Behavior. Physiol. Rev. 82: 637-672, 2002.
Multiple molecular, cellular,
structural, and functional changes occur in the brain during aging.
Neural cells may respond to these changes adaptively, or they may
succumb to neurodegenerative cascades that result in disorders such as
Alzheimer's and Parkinson's diseases. Multiple mechanisms are
employed to maintain the integrity of nerve cell circuits and to
facilitate responses to environmental demands and promote recovery of
function after injury. The mechanisms include production of
neurotrophic factors and cytokines, expression of various cell
survival-promoting proteins (e.g., protein chaperones, antioxidant
enzymes, Bcl-2 and inhibitor of apoptosis proteins), preservation of
genomic integrity by telomerase and DNA repair proteins, and
mobilization of neural stem cells to replace damaged neurons and glia.
The aging process challenges such neuroprotective and neurorestorative
mechanisms. Genetic and environmental factors superimposed upon the
aging process can determine whether brain aging is successful or
unsuccessful. Mutations in genes that cause inherited forms of
Alzheimer's disease (amyloid precursor protein and presenilins),
Parkinson's disease (
-synuclein and Parkin), and trinucleotide
repeat disorders (huntingtin, androgen receptor, ataxin, and others)
overwhelm endogenous neuroprotective mechanisms; other genes, such as
those encoding apolipoprotein E4, have more subtle effects
on brain aging. On the other hand, neuroprotective mechanisms can be
bolstered by dietary (caloric restriction and folate and antioxidant
supplementation) and behavioral (intellectual and physical activities)
modifications. At the cellular and molecular levels, successful brain
aging can be facilitated by activating a hormesis response in which
neurons increase production of neurotrophic factors and stress
proteins. Neural stem cells that reside in the adult brain are also
responsive to environmental demands and appear capable of replacing
lost or dysfunctional neurons and glial cells, perhaps even in the
aging brain. The recent application of modern methods of molecular and
cellular biology to the problem of brain aging is revealing a
remarkable capacity within brain cells for adaptation to aging and
resistance to disease.
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