Alzheimer’s Disease and Parkinson’s Disease: A Nutritional Toxicology Perspective of the Impact of Oxidative Stress, Mitochondrial Dysfunction, Nutrigenomics and Environmental Chemicals

Abstract

Introduction: Alzheimer's disease is primarily a dementia-related disorder from progressive cognitive deterioration and memory impairment, while Parkinson's disease is primarily a movement disorder illness having movement disorder symptoms, bradykinesia (slowness of movements), hypokinesia (reduction of movement amplitude), and akinesia (absence of normal unconscious movements) along with muscle rigidity and tremor at rest. While aging is the main risk factor, epidemiological evidence suggests that the exposure to environmental toxicants, mainly pesticides, metals and solvents could increase the risk of developing neurodegenerative conditions. Oxidative stress in neurodegenerative diseases: Mitochondria function impacts cell respiratory processes, metabolism, energy production, intracellular signaling, free radical production, and apoptosis. In neurodegenerative diseases, mitochondrial dysfunction is associated with a compromised energy production, impaired calcium buffering, activation of proteases and phospholipases, and increased oxidative stress. Oxidative stress induced microglial cells activation, protein aggregation, neuroinflammation and mitochondrial dysfunction lead to neuronal deaths in these disorders. Role of nutrition: Neurodegenerative disease is not curable, but treatment is available to manage the symptoms and slow down the disease progression. The drugs for treating these diseases only reduce the cognitive impairment and behavioral problems, but do not stop the progression of neurodegeneration. Healthy diet, lifestyle improvement and nutraceuticals targeting of oxidative stress, inflammation, abnormal mitochondrial dynamics and the mitochondrial interaction with abnormal diseaserelated proteins and assessment of impact of environmental contaminants including occupational exposures to pesticides, can be a promising approach in the treatment of neurodegenerative diseases. Conclusion: These innovations can be benchmarked on firm understanding of nutrigenomics and the personalized management of individuals at risk.

Cockayne syndrome proteins CSA and CSB maintain mitochondrial homeostasis through NAD+signaling

“…If these processes become uncoordinated, mitochondrial dysregulation can ensue. Hence, mitochondrial dysfunction is causative in many human ailments, including neurological abnormalities [40, 41]. It is important to investigate common phenotypes between human and animal models of CS to explore conserved pathways.…”

The role of nutraceuticals as a complementary therapy against various neurodegenerative diseases: A mini-review

“… 1 , 2 NDDs like PD, AD and, HD can result in dementia and depression and thus contribute to elevated mortality and morbidity, (disabilities) which pose an enormous economical burden. 3 , 4 Also, NDDs are highly connected to aging, and hence the prevalence rate is higher in older people than young owing to decline or altered hormone secretion, enhanced oxidative stress, and, neuro-inflammation. Several studies also demonstrated that NDDs have a direct impact on the social-economic status of any community or country as it hampers cognition and physical (unhealthy aging) or motor movement (quality of life) as well as an incurable condition.…”

Aluminium Binding to Modified Amyloid-β Peptides: Implications for Alzheimer’s Disease

“…Although AD is not curable, some treatments are available to slow down the disease progression and reduce the cognitive impairment and behavioural problems, but do not stop the progression of neurodegeneration [ 38 ]. Our research may show new details about Aβ aggregation and fibrillation associated with AD and highlight the role of aluminium ions in creating a hydrophobic environment that increases the tendency of Aβ peptides to form plaques in AD brains.…”