Proposing Intermittent Fasting as an Approach to Slow Parkinson's Disease Progression
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. On the other hand, mitochondrial dysfunction, oxidative stress, and selective neuronal loss each contribute to PD pathology.
Unfortunately, there remains no disease-modifying treatment in PD despite multiple trials of promising preclinical targets. Supplements and dietary interventions have been periodically considered as possible therapeutic approaches to impact disease progression and severity in related neurodegenerative disorders. One such intervention is intermittent fasting (IF). This viewpoint seeks to describe the putative pathophysiologic relationships among mitochondria, alpha-synuclein, and PD risk genes, and to provide a background for the rationale or the use of IF and similar mitochondrial-targeting therapies in PD. Finally, we propose an outline for determining the efficacy of an IF intervention in PD.
https://medicalxpress.com/news/2021-07-brain-cells-alzheimer-patients-consume.html
a special gene variant causes astrocytes of the brain to exhaust amino acids, essential for neurotransmission. The long-term insufficiency of amino acids may result in compromised neurotransmission and hence cognitive and memory impairments. Findings also indicate that direct brain supplementation of the missing amino acids was effective in alleviating the neurodegenerative outcomes as well as the functional degeneration.