Parkinsons

Parkinson's disease is progressive neurological degenerative state. Discover natural solutions and 17 action steps to improve brain health.

Following reports of low striatal dopamine content in Parkinson’s disease, levodopa was shown to rapidly reverse hypokinesis, establishing the model of disease as one of dopamine deficiency. Dopaminergic therapy became standard of care, yet it failed to reverse the disease, suggesting the understanding of disease was incomplete. The literature suggests the potential for toxicity of dopamine and its metabolites, perhaps more relevant given the recent evidence for elevated cytosolic dopamine levels in the dopaminergic neurons of people with Parkinson’s. To understand the relevance of these data, multiple investigations are reviewed that tested dopamine reduction therapy as an alternative to dopaminergic agents. The data from use of an inhibitor of dopamine synthesis in experimental models suggest that such an approach could reverse disease pathology, which suggests that cytosolic dopamine excess is a primary driver of disease. These data support clinical investigation of dopamine reduction therapy for Parkinson’s disease. Doing so will determine whether these experimental models are predictive and this treatment strategy is worth pursuing further. If clinical data are positive, it could warrant reconsideration of our disease model and treatment strategies, including a shift from dopaminergic to dopamine reduction treatment of the disease.

Right Brain Bio is developing a data-driven treatment for Parkinson's - one so revolutionary that it will transform disease understanding and treatment.

In this podcast episode, Dr. Ardis discusses strategies for preventing and treating Parkinson's disease. He highlights supplements like taurine, selenium, and a foreign protein cleanse as potential ai

For years, the medical community has viewed Parkinson’s Disease (PD) primarily as a neurological disorder, defined by its hallmark motor symptoms such as tremors, rigidity, and postural instability. However, recent …

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PDF | AMPT (alpha-methyl-para-tyrosine) is an inhibitor of tyrosine hydroxylase, the rate-limiting enzyme in dopamine biosynthesis. In clinical... | Find, read and cite all the research you need on ResearchGate

We have already reported that glucosamine (GlcN) distinctly abrogates the pigmentation of human epidermal equivalents stimulated by stem cell factor + endothelin-1 (SE). In this study, we characterized the molecular mechanism involved in the anti-melanogenic effects of GlcN using normal human melanocytes (NHMs) in culture. The SE-stimulated gene (12 h) and protein (24 h) expression levels of melanocyte-specific proteins (at the indicated times post-stimulation) were significantly abrogated by pretreatment with GlcN for 72 h. Western blotting analysis of the phosphorylation of intracellular signaling molecules in the MAPK pathway revealed that despite the significantly decreased level of total CREB protein at all times post-stimulation, the SE-stimulated phosphorylation of ERK, CREB and MITF is not attenuated at 15 min post-stimulation in GlcN-treated NHMs. However, the SE-stimulated protein expression level of total MITF at 2 and 6 h post-stimulation was significantly abrogated by 72 h pretreatment with GlcN. Consistently, pretreatment with GlcN for 72 h abrogated the stimulated gene and protein expression levels of MITF at 1 h and 2 h post-stimulation, respectively. Analysis of gene and protein expression levels also demonstrated that pretreatment with GlcN for 72 h significantly reduced the protein levels of CREB and MITF without affecting their gene expression levels prior to the SE stimulation. Silencing with a CREB siRNA distinctly abrogated the SE-stimulated expression of MITF (at 2 h post-stimulation) and melanocyte-specific proteins (at 24 h post-stimulation). Similarly, transfection of MITF siRNA markedly abrogated the SE-stimulated expression of MITF protein and melanocyte-specific proteins at 2 and 24 h post-stimulation, respectively. Finally, the decreased levels of CREB and MITF proteins induced by 72 h pretreatment with GlcN were abrogated by the co-addition of the proteosomal degradation inhibitor MG132. These findings suggest that the anti-melanogenic effect elicited by GlcN is mediated via the decreased expression of MITF which results from the attenuated transcriptional activity of CREB due to proteolytic degradation.

Intermittent Fasting has been shown to reduce whole body inflammation. Discover how intermittent fasting improves brain function.

The enzyme serrapeptase is used to relieve pain and inflammation; its effects on heart health are also being researched. Learn more here.

Our study demonstrates that systemic trehalose administration preserved the typical histological architecture of the organs involved in its metabolism, supporting its safety as a potential neuroprotective agent.

My current research is on Alzheimer's disease (AD) and Parkinson's disease (PD). I believe that these two diseases are related.

A New & Improved App to Help Track Your Symptoms Each person’s Parkinson’s disease symptoms are different. The more you and your care team know, the more personalized your care can be. The user-friendly APDA Symptom Tracker app helps you capture the details of your symptoms, with new and enhanced features including a medication tracker, notes section, […]

Patients in the PD cohort exhibited distinctive microbiota compositions compared to healthy individuals, with unique differential patterns in gut microbiome abundance at the phylum, family, and genus levels that may be associated wtih PD pathogenesis.

Disease modification in Parkinson's disease (PD) is an unmet medical need. In the current study, we evaluated trehalose, a safe and well-tolerated disaccharide that has previously demonstrated efficacy in rodent models of neurodegenerative diseases, including PD. In a rat model of PD, based on deliv …

Parkinson’s disease (PD) is the second most common neurodegenerative disease in the elderly, which is clinically characterized by bradykinesia, resting tremor, abnormal posture balance, and hypermyotonia. Currently, the pathogenic mechanism of PD remains unclear. Numerous clinical studies as well as animal and cell experiments have found a certain relationship between the vitamin family and PD. The antioxidant properties of vitamins and their biological functions of regulating gene expression may be beneficial for the treatment of PD. Current clinical evidence indicates that proper supplementation of various vitamins can reduce the incidence of PD in the general population and improve the clinical symptoms of patients with PD; nevertheless, the safety of regular vitamin supplements still needs to be highlighted. Vitamin supplementation may be an effective adjuvant treatment for PD. In this review, we summarized the biological correlations between vitamins and PD as well as the underlying pathophysiological mechanisms. Additionally, we elaborated the therapeutic potentials of vitamins for PD.

Contrary to conventional wisdom, brain regeneration is possible. One promising therapy that promotes neurogenesis and is effective in pre-clinical studies of Alzheimer’s and Parkinson’s is near infrared light therapy, and it may improve other mental illnesses and neurodegenerative disorders including dementia, stroke, ALS, and traumatic brain injury as well

Dr. Sarah King, PT, DPT interviews Colin Potter about his experience being diagnosed with Parkinson's Disease and his hard-fought battle to dramatically improve his Parkinson's symptoms. Start building your own Parkinson's Plan of Attack with similar strategies to Colin's: http://www.InvigoratePT.com/start-here LEARN MORE ABOUT SARAH'S PARKINSON'S SPECIFIC EXERCISE PROGRAM: http://www.InvigoratePT.com/Booster FOR ADDITIONAL INTERVIEWS WITH COLIN: http://www.invigoratept.com/blog/colin-potter-fight-parkinsons-special-interview-2017

Could gluten's toxicity extend to the nervous system, producing symptoms identical to classical Parkinson's disease? A compelling case study adds to a growing body of research indicating that wheat's neurotoxicity is greatly underestimated.

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