The effective means of preventing and treating cardio vascular disease diabetes and cancer have been developed. As a result of this average life expectancy has increased from 50 years to 70 years.

This demographic shift of life expectancy has also resulted in occurrence of geriatric related diseases like Alzheimer's disease (AD) and Parkinson's diseases (PD). AD and PD are two diseases that are taking a heavy toll on senior citizens, their relatives and as well health care system. The former American president Ronald Reagan suffered more than a decade and succumbed to AD recently. Neurodegenerative disorders (ND) are proving very difficult to treat and this fact emphasizes the significance to identify ways to slow or prevent these diseases.

There are very few centurions who live free from ND like AD and PD and remain agile and healthy. Although several genetic factors are implicated, recent findings suggest that diet may play a very significant role in brain aging and risk for ND. Epidemiological findings suggest that high calorie diets with folic acid deficiency increase the risk of ND like AD and PD.

Neurodegenerative disorders like AD and PD involves the progressive degeneration and death of neurons. In brain regions such as the hippocampus and basal ganglia in AD and substantia nigra in PD are effected leading to impaired ability of learning, memory and emotional behavior. In PD degeneration of the neurons in substantia nigra results in the patients ability to control body movement. Although AD and PD are usually considered as distinct diseases they share several features of the ND. The common features like increased oxidative stress, metabolic impairment and abnormal protein aggregation, which are easily identifiable. Signs of b amyloid peptide is believed to trigger progression of pathologic consequences like synaptic dysfunction and neuronal death. The b amyloid peptide in the process of aggregation generates free radicals of singlet oxygen, which causes the peroxidation of the membrane lipids leading to the impairment of ATPases and glucose transport proteins. This explains how b amyloid peptide causes the disruption of the ion movement leading to excitatory toxicity and appoptosis of neurons.

Although several genetic factors are implicated, recent finding suggest that diet may play a significant role in brain aging and risk of ND.. Animal model studies on murine have shown the reduced calorie intake or intermittent fasting with folic acid supplementation can slow the progression of pathogenesis of AD and PD. The dietary restrictions on brain result in increased production of neuro trophic factors and cytoprotective protein chaperons in neurons.

The levels of homocystine (HC) in blood increase with age .The persons with elvated HC levels are at high risk of cardiovascular disease like heart attack, stroke. Many patients of AD and PD also have elevated levels of HC. Cells produce HC from amino acid methionin .HC is metabolized by combining of the methyl group by enzymes that require folic acid and cyanocbolamine (vitamin B12 ). HC is also can be made from cystine by an alternate pathway utilizing vitamin B6 .It is converted to cystine by cystothionine b synthase, a vitamin B6 dependent enzyme. Folic acid deficiency can result into hyper homocystinemia.

Studies on animal models of AD and PD have shown that decreasing the HC levels with dietary supplementation of folic acid can be neuro protective.

These findings suggest that HC may intensify the risk of AD and PD by rendering the neurons vulnerable to age related oxidative stress. Folic acid deficiency and HC may endanger neurons by promoting the DNA damage and impairing the repair mechanisms. The intensified DNA damage may ultimately trigger appoptosis leading to neuronal death. Hence it is suggestive that dietary factors may interact with disease causing or predisposing genes in molecular cascades that either promote or prevent the degeneration of the neurons.

Summary of findings regarding relationship between elvated HC and folic acid deficiency as risk factors for AD and PD
§ Low calorie intake associated with reduced risk of ND.
§ Calorie restriction preserves memory in aging in rodents and has anti aging effects.
§ Dietary restrictions has neuro protective action on rodents models of AD and PD.
§ Folate levels are decreased and HC levels increased in patients with AD and PD.
§ High HC levels are associated with poor cognitive functions.
§ Neuron protective action of folic acid and elevated HC levels endanger neurons in animal models of AD and PD.

Mahatma Gandhi who practiced intermittent fasting might have escaped the ND due to his highly disciplined dietary habits. The Ekadasi practice of intermittent fasting and fasting during the holy month of Ramzan is some of the ethnic practices of intermittent fasting which our ancestors practiced religiously from time immemorial might have helped them to escape from ND. All these suggest calorie conscious diet with folic acid supplement and intermittent fasting should become the habit of the aged one as this would act as a prophylactic for ND, Cardiovascular diseases and diabetes.

-- The author is with Pharmacy Group, Birla Institiute of Science and Technology, Pilani