Medical & Clinical Reviews

Description

With the exception of Alzheimer's disease, Parkinson's Disease (PD) is the most prevalent neurodegenerative disease. It is characterized by the pigmented, dopamine-containing neurons in the substantia nigra pars compacta slowly deteriorating over time. Other dopaminergic neurons also degenerate, albeit to a lesser extent. A movement disorder with the classic parkinsonian motor signs of bradykinesia, muscular rigidity, rest tremor and impairment of posture and gait results from the dopamine deficiency in the basal ganglia. Non-motor symptoms include cognitive impairments, olfactory dysfunction, psychiatric changes, autonomic dysfunction, and insomnia in people with PD; some of these symptoms may occur years before motor dysfunction. The accumulation of a protein that has been misfolded, -synuclein, in Lewy bodies and Lewy neurites is the neuropathological hallmark of PD. These poisonous considerations are related with neurodegenerative changes basically in the dopaminergic nigrostriatal framework, yet in addition in the locus coeruleus as well as in cortical and limbic regions. Maturing is the significant gamble element of PD, which influences roughly 1% of grown-ups more seasoned than 60 years. It is believed that people in their early to mid-60s are most likely to develop PD. The onset of symptoms in people with PD can occur between the ages of 21 and 40 or before the age of 20, depending on the type of PD. Oxidative stress, mitochondrial dysfunction, and abnormal aggregation of beta-synuclein are all pathophysiological mechanisms in PD. Because it uses a lot of oxygen, has a lot of iron, and has unsaturated fatty acids, which are targets for lipid peroxidation, the brain is especially vulnerable to oxidative damage. Irritation might assume a part in both the commencement and movement of α-synuclein collection. Although the cause of Parkinson's disease (PD) is unknown, it appears to involve a complicated interaction between genetic and environmental factors. In only a small percentage of cases, the genes known to be associated with PD can be causally linked to the disease. Organochlorines and other pesticides appear to play a role in the development of Parkinson's disease in relation to environmental factors. Recent findings support the hypothesis that pathological changes in PD may spread from the intestinal tract to the brain via the vagus nerve, despite the fact that the reason for the brain's neuronal loss in PD is still poorly understood. This hypothesis is further supported by the discovery of aggregations of -synuclein in the salivary glands and intestinal mucosa at least a decade prior to the onset of motor symptoms in people with Parkinson's disease and the nearly 50% reduction in the risk of developing the disease in people who had undergone vagotomy as a therapeutic intervention for peptic ulcer.

Etiology of Parkinson's Disease

The etiology of Parkinson's Disease (PD) may be influenced by particular macro and micronutrients. A model outlining the impact of food admission on the event of parkinsonism is the amyotrophic parallel sclerosis-parkinsonism/dementia complex found chiefly in Guam, the reason for which is the utilization of neurotoxic cycad seeds. An expanded utilization of milk and dairy items has been accounted for in a few planned partner studies to be related with a raised gamble of PD. For instance, the results of two large prospective cohort studies with over 125,000 participants and at least 24 years of follow-up were used to investigate this connection. While the consumption of skim and low-fat milk and other low-fat dairy products was found to be associated with PD risk in both men and women, the total intake of dairy products did not significantly increase the risk. A meta-analysis of prospective cohort studies also suggests that dairy products may be linked to a higher risk of Parkinson's disease. According to the linear dose–response relationship, the risk of Parkinson's disease rose by 17% for every 200 g/day increase in milk intake and by 13% for every 10 g/day increase in cheese intake. Omega-3 PUFAs act as energy substrates and layer parts, and assume a fundamental part in keeping up with undisturbed neurobiological capabilities. It has been demonstrated that omega-3 PUFAs perform a wide range of functions that may be relevant to the neurodegenerative process in Parkinson's disease. These include encouraging actions that reduce oxidative stress, inflammation, neurotrophic factors, apoptosis, and inflammation. A crucial neurosteroid, vitamin D is necessary for brain development and function. A wide range of neurological conditions, including multiple sclerosis, stroke, and neurodegenerative diseases, have been linked to vitamin D deficiency. Numerous parts of the human brain contain vitamin D receptors and the enzyme 1-alphahydroxylase, which makes vitamin D work. Globally, B vitamin deficiency is a frequent cause of neurological impairment and disability. Homocysteine, a metabolite of the essential amino acid methionine cycle, provides the basis for the hypothesis that B vitamins play a role in Parkinson's Disease (PD). Homocysteine shows numerous neurotoxic pathogenetic impacts in neurodegenerative issues, including PD. Homocysteine levels are higher in people with PD than in healthy people their age. Through neurotoxic effects, elevated homocysteine levels may accelerate dopaminergic cell death in Parkinson's Disease (PD), whereas plasma homocysteine levels may reduce the risk of PD.

Role of Diet in the Pathogenesis of PD

These food bioactives have been hypothesized to protect against PD because dietary antioxidants like vitamins C, E, and carotenoids, which can prevent oxidative damage, appear to play a role in neurodegeneration in Parkinson's disease. In order to meet the specific dietary requirements of people who suffer from metabolic disorders or other diseases, medical foods, also known as foods made specifically for medical purposes, are produced using a particular processing formula. In the US, a clinical food is characterized as "a food which is formed to be devoured or directed enterally under the oversight of a doctor and which is expected for the particular dietary administration of an illness or condition for which unmistakable healthful necessities, in view of perceived logical standards, are laid out by clinical assessment. The development of treatments to halt or delay the disease's progression has not progressed, despite significant advancements in PD symptomatic therapy. The majority of the drugs currently used to treat Parkinson's disease dopamine replenishment and symptom relief in the early stages of the disease. However, these medications neither halt nor halt the progression of PD. Dietary factors may be one modifiable lifestyle factor linked to a lower rate of PD progression. With plausible biological hypotheses, a variety of foods and nutrients have been suggested as potential risk factors for Parkinson's disease. The role of diet in the pathogenesis of PD may be limited given that the majority of single food groups did not predict the occurrence of PD. Be that as it may, enormous forthcoming examinations should be directed to explain this issue.