Gluten related PD

Gluten ataxia
File:Gluten ataxia eng.ogv
en.wikipedia.org/wiki/Gluten

Gluten ataxia is an autoimmune disease triggered by the ingestion of gluten.[75] With gluten ataxia, damage takes place in the cerebellum, the balance center of the brain that controls coordination and complex movements like walking, speaking and swallowing, with loss of Purkinje cells. People with gluten ataxia usually present gait abnormality or incoordination and tremor of the upper limbs. Gaze-evoked nystagmus and other ocular signs of cerebellar dysfunction are common. Myoclonus, palatal tremor, and opsoclonus-myoclonus may also appear.[76]

Early diagnosis and treatment with a gluten-free diet can improve ataxia and prevent its progression. The effectiveness of the treatment depends on the elapsed time from the onset of the ataxia until diagnosis, because the death of neurons in the cerebellum as a result of gluten exposure is irreversible.[76][77]

Gluten ataxia accounts for 40% of ataxias of unknown origin and 15% of all ataxias.[76][78] Less than 10% of people with gluten ataxia present any gastrointestinal symptom, yet about 40% have intestinal damage.[76]

Other neurological disorders
In addition to gluten ataxia, gluten sensitivity can cause a wide spectrum of neurological disorders, which develop with or without the presence of digestive symptoms or intestinal damage.[13] These include peripheral neuropathy, epilepsy, headache, encephalopathy, vascular dementia, and various movement disorders (restless legs syndrome, chorea, parkinsonism, Tourette syndrome, palatal tremor, myoclonus, dystonia, opsoclonus myoclonus syndrome, paroxysms, dyskinesia, myorhythmia, myokymia).[13][79]

The diagnosis of underlying gluten sensitivity is complicated and delayed when there are no digestive symptoms. People who do experience gastrointestinal problems are more likely to receive a correct diagnosis and treatment. A strict gluten-free diet is the first-line treatment, which should be started as soon as possible. It is effective in most of these disorders. When dementia has progressed to an advanced degree, the diet has no beneficial effect. Cortical myoclonus appears to be treatment-resistant on both gluten-free diet and immunosuppression.[13]

Toxic Chemicals, Plants, and Organic Elements that may Trigger Development of PD

Viartis is a UK-based group of independent, self-funded medical researchers specializing in Parkinson’s Disease. They have compiled a list of toxic elements that may cause or partially cause PD. The list includes plants and flowers like Annonaceae; chemical elements like Carbon Disulfide, copper, and cyanide; pesticides like Dieldrin; organic compounds like Hydrocarbons and industrial chemicals like N-Hexane. Each toxic element is given a brief description and a list of where you might be exposed to the dangerous element. It includes mention of consumer products that may contain the chemicals and where they come from. High exposure to these toxic substances has been found to increase the chances of developing PD.

Source: Toxic Causes of PD

Detox options, click here

Toxins used in labs to generate PD model

Could Parkinson’s be Caused by Infection?

In examining the hypothesis that PD could stem from an influenza virus infection that develops into encephalitis lethargica the role of bacterial and viral infections as a possible cause of Parkinsonism is questioned. The paper compares the clinical, histological, and structural features of Parkinsonism in infectious diseases and looks at the influenza virus and why and how it became associated with PD. Herpes Simplex Virus 1; Epstein-Barr Virus; Varicella-Zoster Virus; Hepatitis C; the Japanese Encephalitis Virus and the West Nile Virus are discussed in connection with PD. The review also examines the Human Immunodeficiency Virus (HIV) and Parkinsonism. In conclusion, the synergistic effect of infectious pathogens in inducing neuroinflammation leading to PD development has been observed. However, it cannot be established that all cases of PD are associated with increased inflammation and underlying chronic infection. Further research is necessary to examine the involvement and extent to which pathogens and inflammatory cytokines play in the pathomechanism of PD.

Source: Infectious Etiologies of Parkinsonism: Pathomechanisms and Clinical Implications

The Link Between Helicobacter Pylori and PD?

This 2018 report from the Journal of Parkinson’s Disease examines the association between the gut bacteria Helicobacter pylori and PD. H. pylori is a common gut bacterium that causes ulcers, gastritis, and can lead to stomach cancer. The majority of PD cases are caused by unknown environmental factors, and bacterial infections could be one of them. This has led doctors to look at the link between H. pylori and PD. After reviewing past studies on the subject four important points were noted: H. pylori-infected PD patients experience worse motor function issues than those not infected; people with PD are more prone to be infected by H. pylori and eradication of H. pylori could improve motor function and levodopa absorption in people with PD.

Source: Eradicating Helicobacter pylori Infections May Be a Key Treatment for Parkinson’s Disease

Can RYR supplements Potentially be Related to a High Risk of PD?

Red yeast rice (RYR or red Koji) is an ingredient in dietary supplements often used for people with dyslipidemia or with statin-intolerance. These supplements contain monacolin K (lovastatin). This 2017 study published by NCBI made a case-by-case assessment highlighting myopathies and liver injury as potential safety issues, thus suggesting that the safety profile of RYR is similar to statins. RYR is used in Chinese medicine as a natural statin to improves blood circulation by decreasing cholesterol and triglyceride levels. Certain studies have shown that statin use and a higher risk of PD are related and that PD symptoms appear to be stronger following use of statins. These findings raise the hypothesis that the safety profile of RYR is highly similar to that of synthetic statins and warrants further investigation to finally characterize the safety profile of RYR. The conclusion of this report is that the safety profile of RYR is similar to that of statins and the risk profile of these supplements needs to be examined and regulated.

Source: Adverse reactions to dietary supplements containing red yeast rice: assessment of cases from the Italian surveillance system

Neuronal Autophagy and the Predisposition for PD

A study by Dr. Yue published by the Michal J. Fox Foundation tested the hypothesis that neuronal autophagy is critical for the regulation of alpha-synuclein protein levels and protective against neuronal death; dysfunction of autophagy predisposes to the pathogenesis of PD in dopamine neurons. This was done by establishing conditional knock-out mice in which an essential autophagy gene, Atg7, is deleted specifically in dopamine neurons. These pre-clinical models were used to investigate whether alpha-synuclein wildtype or PD-mutant A53T will be accumulated and deposited into Lewy body-like inclusions in the mutant dopamine neurons. In addition, they studied the effect of inactivation of autophagy on oxidative stress level, striatal dopamine content, and dopamine neuron degeneration. results suggest that neuronal autophagy is critical for the regulation of alpha-synuclein protein levels and protective against neuronal death; dysfunction of autophagy may predispose dopamine neuron to PD-like pathology.

Source: Autophagy in Dopamine Neurons: Clearance of Alpha-synuclein and Neuroprotection

PD and Autophagy Impairment in Synucleinopathy

A 2019 study published by NCBI discusses the active participation of autophagy impairment in alpha-synuclein accumulation and propagation, as well as alpha-synuclein-independent neurodegenerative processes in the field of synucleinopathy. There is genetic and post-mortem evidence suggesting that autophagy is involved in synucleinopathies. Also, studies demonstrate the role of autophagy in the pathology of synucleinopathy. α-syn is mainly degraded by both macroautophagy and chaperone-mediated autophagy. Thus, autophagy defects induce intracellular α-syn accumulation, participating in its aggregative state towards the formation of α-syn-positive intracytoplasmic inclusions. Plus, autophagy defects also increase the α-syn secretion by the non-autophagic exosomal pathway, leading to increased cell-to-cell transmission of the protein, and thus the propagation of the α-syn-linked pathology in different brain regions of the CNS. However, autophagy defects also cause detriment effects in cellular homeostasis: (i) lysosomal impairment through structural or functional defects leads to accumulation of non-degraded products and increased production of ROS; (ii) decreased mitophagy leads to neuronal bioenergetic imbalance, and (iii) defective cargo trafficking impairs the addressing of vesicles to lysosomal clearance. There is increasing evidence that inducing the autophagy pathways (by natural, chemical, or genetic approaches), has become a relevant therapeutic approach to counteract the deleterious effects of autophagy impairment in synucleinopathy.

Source: Autophagy in Synucleinopathy: The Overwhelmed and Defective Machinery

Vitamin D | Linus Pauling Institute | Oregon State University

n a randomized, double-blind, placebo-controlled study, 112 PD patients (mean age, 72 years) on standard PD treatment were supplemented with 1,200 IU/day of vitamin D or a placebo for 12 months. Vitamin D supplementation nearly doubled serum 25-hydroxyvitamin D concentration (from mean of 22.5 ng/mL to 41.7 ng/mL) in supplemented subjects and limited the progression of PD, as indicated by a greater proportion of patients who showed no worsening (as assessed by the Hoehn and Yahr stage and the United Parkinson Disease Rating Scale part II) in the supplemented group compared to the placebo group (243). It is not known whether vitamin D insufficiency has a role in the pathogenesis of the disease, but the repletion of vitamin D may provide health benefits that go beyond the prevention and/or the treatment of PD. For example, vitamin D deficiency may contribute to the increased risk of osteoporosis and bone fracture in individuals with neurologic disorders, including PD and multiple sclerosis (244-246). Interestingly, sunlight exposure was found to be associated with improved vitamin D status, higher bone mineral density of the second metacarpal bone, and lower incidence of hip fracture in a prospective study conducted in 324 elderly people with PD (247).

Source: Vitamin D | Linus Pauling Institute | Oregon State University