A metabolic and functional overview of brain aging linked to neurological disorders.
Close correlations have recently been shown among the late onset complications encountered in diabetes and aging linked to neurobiological disorders. Aging in females and males is considered as the end of natural protection against age related diseases like osteoporosis, coronary heart disease, diabetes, Alzheimer's disease and Parkinson's disease, dementia, cognitive dysfunction and hypernatremia. Beside the sex hormones other hormonal changes are also known to occur during aging and many common problems encountered in the aging process can be related to neuroendocrine phenomena. Diabetes mellitus is associated with moderate cognitive deficits and neurophysiologic and structural changes in the brain, a condition that may be referred to as diabetes encephalopathy; diabetes increases the risk of dementia especially in the elderly. The current view is that the diabetic brain features many symptoms that are best described as accelerated brain aging. This review presents and compares biochemical, physiological, electrophysiological, molecular, and pathological data from neuronal tissue of aging and hormone treated control and diabetic animals to arrive at the similarities among the two naturally occuring physiological conditions. Animal models can make a substantial contribution to understanding of the pathogenesis, which share many features with mechanism underlying brain aging. By studying the pathogenesis, targets for pharmacology can be identified, finally leading to delay or prevention of these complications. Antiaging strategies using hormone therapy, chemical and herbal compounds were carried out for reversal of aging effects. Neuronal markers have been presented in this review and similarities in changes were seen among the aging, diabetes and hormone treated (estrogen, DHEA and insulin) brains from these animals. A close correlation was observed in parameters like oxidative stress, enzyme changes, and pathological changes like lipofuscin accumulation in aging and diabetic brain.
Baquer
Najma Z
NZ
School of Life Sciences, Jawaharlal Nehru University, New Delhi, India. nzbaquer@gmail.com
Taha
Asia
A
Kumar
Pardeep
P
McLean
P
P
Cowsik
S M
SM
Kale
R K
RK
Singh
R
R
Sharma
Deepak
D
D000200:Action Potentials; D000367:Age Factors; D000375:Aging / Q000378:metabolism*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001921:Brain / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D016922:Cellular Senescence / Q000187:drug effects; D003071:Cognition; D048909:Diabetes Complications / Q000378:metabolism* / Q000503:physiopathology / Q000517:prevention & control / Q000523:psychology; D005260:Female; D005947:Glucose / Q000378:metabolism; D012739:Gonadal Steroid Hormones / Q000378:metabolism; D006801:Humans; D008297:Male; D009422:Nervous System Diseases / Q000378:metabolism* / Q000503:physiopathology / Q000517:prevention & control / Q000523:psychology; D018696:Neuroprotective Agents / Q000494:pharmacology; D018384:Oxidative Stress; D036361:Peptide Hormones / Q000378:metabolism
D000975:Antioxidants; D012739:Gonadal Steroid Hormones; D018696:Neuroprotective Agents; D036361:Peptide Hormones; D005947:Glucose