Saturday, October 25, 2008

Brain Aging in Relation to Genes, Diet, and Behavior

Over recent years there has been tremendous progress in our understanding of brain aging and neurodegeneration. Whereas in times past it was presumed that little could be done to forestall the onset of age associated cognitive impairment it is now obvious that there is a welter of strategies we can utilise to markedly slow down the rate of age associated cognitive impairment.

This review article from Mark P. Mattson et. al. is a good starting point for enhancing your understanding of brain aging and the strategies that can help in slowing that trend. Some even claim that one can completely forestall brain aging. I remain very cynical of that possibility but hey it is worth a try so give it a go!

In brief, the following strategies are advisable:

  • Regular light aerobic exercise.
  • Moderate fasting a couple of times a week appears to be beneficial. Caloric Restriction, however, is ill advised as there is some suggestion that over the long term it can damage the brain.
  • A good diet, obviously.
  • Avoiding saturated fats and trans fats. Do not eliminate saturated fat, just reduce it.
  • Maintaining an appropriate balance of omega 3 to omega 6 fats.
  • Regular sleeping patterns.
  • Avoiding excessive stress.
  • Treat depression quickly. Numerous studies now indicate that depression damages the brain and the body. In fact sustained major depression is a significant risk factor for Alzheimers and a minor risk factor for heart disease.
  • Avoid knocks to the head. Even mild brain injury can pave the way for latter dementia.

The abstract:

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; 10.1152/physrev.00004.2002.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 (alpha -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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