Intermittent fasting strategies, such as alternate day fasting, are known to slow aging in a variety of species. The mechanisms are likely similar to those involved in the calorie restriction response, meaning upregulation of stress responses and cellular maintenance, though intermittent fasting is capable of producing some degree of benefits even when overall calorie intake is not reduced. Time spent in a state of hunger, and the consequent reactions of cells and tissues, is clearly an important factor. The human data for both calorie restriction and intermittent fasting shows health benefits, and from what is known of the mechanisms involved it is reasonable to propose that calorie restriction or intermittent fasting could modestly slow at least some forms of neurodegenerative condition.
Parkinson’s disease (PD) is the second most common neurodegenerative disease, affecting ~2% of the population over age 70. Disease prevalence increases with age and, given the aging population, may triple in the next few years. The neurodegenerative mechanism leading to PD is still not completely elucidated. Alpha-synuclein may drive the neurodegenerative process of PD. When aggregated in neurons as intracellular Lewy bodies, it constitutes the pathologic hallmark of PD.
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