Parkinsons

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 …

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.

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

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

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.

(NaturalHealth365) As evidence of the weed killer’s toxicity continues to pour in, the EPA turns its head and supports the use of paraquat.

Microbiota-gut-brain axis, the bidirectional relationship between the gut microbiota and the brain, has been increasingly appreciated in the pathogene…

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.

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.

We now can convincingly demonstrate that a ketogenic diet is helpful in Parkinson’s, and we now have a better understanding of the underlying mechanisms.

Parkinson's disease (PD) is the second most common neurodegenerative disorder of aging. The pathological hallmark of PD is neuronal inclusions termed Lewy bodies whose main component is alpha-synuclein protein. The finding of these Lewy bodies in the intestinal enteric nerves led to the hypothesis that the intestine might be an early site of PD disease in response to an environmental toxin or pathogen. One potential mechanism for environmental toxin(s) and proinflammatory luminal products to gain access to mucosal neuronal tissue and promote oxidative stress is compromised intestinal barrier integrity. However, the role of intestinal permeability in PD has never been tested. We hypothesized that PD subjects might exhibit increased intestinal permeability to proinflammatory bacterial products in the intestine. To test our hypothesis we evaluated intestinal permeability in subjects newly diagnosed with PD and compared their values to healthy subjects. In addition, we obtained intestinal biopsies from both groups and used immunohistochemistry to assess bacterial translocation, nitrotyrosine (oxidative stress), and alpha-synuclein. We also evaluated serum markers of endotoxin exposure including LPS binding protein (LBP). Our data show that our PD subjects exhibit significantly greater intestinal permeability (gut leakiness) than controls. In addition, this intestinal hyperpermeability significantly correlated with increased intestinal mucosa staining for E. coli bacteria, nitrotyrosine, and alpha-synuclein as well as serum LBP levels in PD subjects. These data represent not only the first demonstration of abnormal intestinal permeability in PD subjects but also the first correlation of increased intestinal permeability in PD with intestinal alpha–synuclein (the hallmark of PD), as well as staining for gram negative bacteria and tissue oxidative stress. Our study may thus shed new light on PD pathogenesis as well as provide a new method for earlier diagnosis of PD and suggests potential therapeutic targets in PD subjects. Trial Registration Clinicaltrials.gov NCT01155492

Parkinson's disease (PD) is the second most common neurodegenerative disorder of aging. The pathological hallmark of PD is neuronal inclusions termed Lewy bodies whose main component is alpha-synuclein protein. The finding of these Lewy bodies in the intestinal enteric nerves led to the hypothesis that the intestine might be an early site of PD disease in response to an environmental toxin or pathogen. One potential mechanism for environmental toxin(s) and proinflammatory luminal products to gain access to mucosal neuronal tissue and promote oxidative stress is compromised intestinal barrier integrity. However, the role of intestinal permeability in PD has never been tested. We hypothesized that PD subjects might exhibit increased intestinal permeability to proinflammatory bacterial products in the intestine. To test our hypothesis we evaluated intestinal permeability in subjects newly diagnosed with PD and compared their values to healthy subjects. In addition, we obtained intestinal biopsies from both groups and used immunohistochemistry to assess bacterial translocation, nitrotyrosine (oxidative stress), and alpha-synuclein. We also evaluated serum markers of endotoxin exposure including LPS binding protein (LBP). Our data show that our PD subjects exhibit significantly greater intestinal permeability (gut leakiness) than controls. In addition, this intestinal hyperpermeability significantly correlated with increased intestinal mucosa staining for E. coli bacteria, nitrotyrosine, and alpha-synuclein as well as serum LBP levels in PD subjects. These data represent not only the first demonstration of abnormal intestinal permeability in PD subjects but also the first correlation of increased intestinal permeability in PD with intestinal alpha–synuclein (the hallmark of PD), as well as staining for gram negative bacteria and tissue oxidative stress. Our study may thus shed new light on PD pathogenesis as well as provide a new method for earlier diagnosis of PD and suggests potential therapeutic targets in PD subjects. Trial Registration Clinicaltrials.gov NCT01155492

Sarah King, PT, DPT shows people diagnosed with Parkinson's Disease how to create a personalized Parkinson’s action plan that improves their symptoms, so they can spend less time worrying and more time doing the things they love, with the people they love, for as long as possible.

Science says eating just one meal per day can improve your health. Learn more at https://highintensityhealth.com/OMAD ----- Connect with Bill Curtis: https://www.thefourthfoodgroup.com/ Related Video testing the KetoAid Ketone Ester: https://youtu.be/V-ILObXYsaQ This episode is brought to you by: ➢ Health IQ, an insurance company that helps health conscious people like weightlifters, cyclist, keto dieters and vegetarians get lower rates on their life insurance. ➢ Get a Free Quote: http://healthiq.com/HIH Somnifix.com, the world’s only hypoallergenic mouth tape, developed by Harvard Scientists. https://www.somnifix.com Key Timestamps: 01:55 Journalist Bill Curtis has had Parkinson's since 2000. As predicted, he was dramatically affected 10 years later with advanced Parkinson's. Now the only symptom he has is a slight tremor. 04:48 Within about 2 hours of eating carbs, Bill will begin to shake and feel rigid. He doesn't get the full on symptoms he had before. 07:38 Bill was in an exercise program. In an attempt to enhance the effects of the program, he fasted overnight and had nothing for breakfast before the workout. He found it alleviated his profound fatigue. 11:27 Fasting helped with the fatigue, but there were many more symptoms that were not reversed. Bill continued researching. 13:02 Bill exercised fasted every day for a year. He lost weight, but eventually, it stopped working. As you become fit, you make fewer ketones. 15:04 Dr. Veech suggested that Bill try Bulletproof Coffee after the night fast. Nearly all of his symptoms abated at the end of the first hour. 19:36 The military has been experimenting with Dr. Veech's ketone ester for radiation exposure. 22:26 A therapeutic ketogenic diet is one with 80 to 90% of your food as fat. Bill has devised 4 levels of ketosis. 30:33 Within the first 10 days of taking ketone ester, Bill no longer had urinary incontinence. 32:07 There is data that an elevation of uric acid it will delay the onset of Parkinson's. If you have Parkinson's, and your uric acid levels are higher, you decline more slowly. 36:14 BHB allows you to make more dopamine, serotonin, adrenaline, noradrenaline and nitric oxide. 38:00 In advanced Parkinson's neurotransmitters are negatively impacted. With ketosis, you are making serotonin, noradrenaline, adrenaline, dopamine and nitric oxide synthase. 38:52 Every antioxidant has to be recharged with an electron from NADPH, directly or indirectly. 39:50 Beta hydroxybutyrate raises NADPH levels using isocitrate dehydrogenase in the cytoplasm, outside of the mitochondria. 42:24 NADPH levels in the mitochondria does not correlate with NADPH levels in the cytosol. We should measure the cytosolic NADPH. 44:09 NADPH voltage is dependent upon the relative concentrations. More equals more resilience. 48:52 Dismutase does not get its electrons from the battery. It does this by taking 2 molecules of superoxide, oxidizing one and reducing the other. 52:59 You have the ability to use ketones to restore ischemia-reperfusion and turn off inflammation. 54:08 NADPH controls inflammation. 55:04 Dr. Veech found that treating Alzheimer's mouse models with beta hydroxybutyrate kept them from accumulating beta amyloid deposits. 58:03 Bill believes that TBI will respond very well to BHB, as evidenced by people close to him with head injuries. 01:02:41 Bill has created an online course to help people help each other. You need a cook, a coach, a nutritionist and a doctor. 01:04:36 Bill must still take his Parkinson's medications.

The low-carb keto diet gets debunked once and for all! For more information head over to masteringdiabetes.org WIN THE OPPORTUNITY TO STUDY PLANT BASED NUTRITION COURSE WITH ECORNELL - www.plantbasednews.org/competitions/win-with-pbn --- ★ SUPPORT OUR WORK BY MAKING A CONTRIBUTION: https://www.plantbasednews.org/support ★ GET OUR FREE MEAL INSPIRATION GUIDE: http://bit.ly/pbnmealguide ★ HELP TRANSLATE OUR VIDEOS: http://bit.ly/translatePBN ★ SIGN UP TO RECEIVE OUR WEEKLY HEADLINES IN YOUR INBOX: http://www.plantbasednews.org/signup ★ GOT A NEWS STORY WE SHOULD KNOW ABOUT? Please email press@plantbasednews.org or leave a message on our hotline UK landline: +44 207 0960 175, US landline: +1 818 963 5411 ★ CHECK OUT OUR WEBSITE: http://www.plantbasednews.org/ SOCIAL MEDIA ★ TWITTER: https://www.twitter.com/plantbasednews ★ FACEBOOK: https://www.facebook.com/plantbasednews ★ YOUTUBE: https://www.youtube.com/plantbasednews ★ INSTAGRAM: https://www.instagram.com/plantbasednews LEARN ABOUT VEGANISM ★ Cowspiracy ➞ https://youtu.be/nV04zyfLyN4 ★ NutritionFacts.Org ➞ https://goo.gl/BdNbiU ★ Veganuary ➞ http://www.veganuary.com/