Dramatic Recovery In Parkinson’s Patient with Gluten Free Diet
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.
Benefits of Vitamins in the Treatment of Parkinson’s Disease
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.
Beneficial effects of trehalose on striatal dopaminergic deficits in rodent and primate models of synucleinopathy in Parkinson's disease. - PubMed - NCBI
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 …
Glucosamine abrogates the stem cell in human melanocytes
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.
Fulvic acid inhibits aggregation and promotes disassembly of tau fibrils associated with Alzheimer's disease. - PubMed - NCBI
Alzheimer's disease is a neurodegenerative disorder involving extracellular plaques (amyloid-β) and intracellular tangles of tau protein. Recently, tangle formation has been identified as a major event involved in the neurodegenerative process, due to the conversion of either soluble peptides or oli …
Home - Muses Labs - MEND™ Protocol for Alzheimer’s disease
Muses Labs, partnering with leading Alzheimer's researchers, pioneered the MEND™ Protocol to treat underlying drivers of Alzheimer’s disease with big-data.
How to Stop Dementia and Alzheimer's Naturally - YouTube
Dementia and Alzheimer's a big problem in industrialized countries. With the aging population at greater and greater risk for these conditions, it is imperative to understand that there are a variety of natural ways to stop dementia in its tracks. In this video, Dr. Osborne breaks down 6 natural ways you can overcome brain inflammation (brainflammation) including:
1. Avoid gluten
2. Eat lots of healthy fats
3. Avoid eating excessive carbohydrates
4. Take exercise more seriously
5. Maintain a healthy blood sugar
6. Do a medication review with your doctor.
Remember, natural help is all about your diet and your lifestyle. There are no magic cures. You have to put in the work.
To connect with Dr. Osborne visit:
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Twitter: https://twitter.com/glutenology
*These statements have not been evaluated by the Food and Drug Administration. This video is not intended to diagnose, treat, cure or prevent any disease. It is strictly intended for educational purposes only. Additionally, this information is not intended to replace the advice of your physician. Dr. Osborne is not a medical doctor. He does not treat or diagnose disease. He offers nutritional support to people seeking an alternative from traditional medicine. Dr. Osborne is licensed with the Pastoral Medical Association.
Human amyloid-beta acts as natural antibiotic in the brain Alzheimer's (...)
A new study provides additional evidence that amyloid-beta protein -- which is deposited in the form of beta-amyloid plaques in the brains of patients with Alzheimer's disease -- is a normal part of the innate immune system, the body's first-line defense against infection.
Leaky blood-brain barrier linked to Alzheimer's disease -- ScienceDail (...)
Researchers using contrast-enhanced MRI have identified leakages in the blood-brain barrier of people with early Alzheimer's disease, according to a new study. The results suggest that increased BBB permeability may represent a key mechanism in the early stages of the disease.
Link between brain, bone in Alzheimer's disease identified -- ScienceD (...)
Researchers have identified a major connection between areas of the brainstem - the ancient area that controls mood, sleep and metabolism - and detrimental changes to bone in a preclinical model of Alzheimer's disease.
Link between gum disease and cognitive decline in Alzheimer’s -- Scien (...)
A new study has found a link between gum disease and greater rates of cognitive decline in people with early stages of Alzheimer's Disease.Periodontitis or gum disease is common in older people and may become more common in Alzheimer's disease because of a reduced ability to take care of oral hygiene as the disease progresses. Higher levels of antibodies to periodontal bacteria are associated with an increase in levels of inflammatory molecules elsewhere in the body, which in turn has been linked to greater rates of cognitive decline in Alzheimer's disease in previous studies. The latest study set out to determine whether periodontitis or gum disease is associated with increased dementia severity and subsequent greater progression of cognitive decline in people with Alzheimer's disease.
Lipid-based diets effectively combat Alzheimer's disease in mouse mode (...)
Researchers have devised several lipid-based diets aimed at slowing down progression and relieving symptoms of Alzheimer's disease (AD). It is generally accepted that lifestyle and particularly dietary habits influence mental health, and prevalence and progression of AD. Numerous epidemiological studies have revealed profitable effects of dietary intake of especially fish oil on cognitive decline during aging and dementia.
Marijuana Compound Found Superior To Drugs For Alzheimer's
Could the active ingredient in marijuana, responsible for its characteristic "high," help turn the tide against the accelerating Alzheimer's epidemic? A remarkable study published in the journal Molecular Pharmacology in 2006, found that this long vilified plant may contain a compound with not one, but two therapeutic properties ideal for addressing both the surface symptom (memory problems) and root cause (brain plaque) of Alzheimer’s disease
Mitophagy and Alzheimer’s disease cellular and molecular mechanisms
Neurons affected in Alzheimer’s disease (AD) experience mitochondrial dysfunction and a bioenergetic deficit that occurs early and promotes the disease-defining amyloid β-peptide (Aβ) and Tau pathologies. Emerging findings suggest ...