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

Could Intermittent Fasting/ Caloric Restriction/ Exercise Improve PD Status

This review was written by Dr. Mark P. Mattson of the John Hopkins University School of Medicine and published in the 2014 Journal of Parkinson’s Disease. It examines whether lifestyle changes that increase insulin sensitivity such as increased exercise and intermittent energy restriction (intermittent fasting)  could counteract neurodegenerative processes and improve functionality. Various studies on animal models seem to indicate that peripheral insulin resistance and midlife diabetes may increase the risk of PD. This review examines whether improved peripheral and brain energy metabolism, exercise, GLP-1 analogs, and intermittent energy restrictions (IER) could boost neuronal adaptive stress response pathways and ultimately enhance neurotrophic signaling, DNA repair, mitochondrial biogenesis, and proteostasis.

Interventions that Improve Body and Brain Bioenergetics for Parkinson’s Disease Risk Reduction and Therapy by Dr Mark Mattson
Mark Mattson in TED: fasting/caloric restriction/ intermittent fasting…help against neurodegenerative conditions

In Development: Neuralink’s Brain Implants , to Treat PD

The latest invention from Neuralink is ultra-thin “threads” that could be injected into the brain to examine neuron activity. These brain-chip interfaces could hopefully be used to treat chronic conditions like PD. One of the goals of this new technology is to allow humans to keep up with the constant leaps and bounds of AI tech. So far there have only been animal trials of Neuralink’s new technology but with astounding results. Neuralink president, Max Hodak said that the company is close to clinical trials in neurological disorders.

The first human trials will focus on paralysis patients and will involve installing four of the new devices into the patient’s brains. If successful, Neuralink will probably release some developer API. The new technology has the potential for use on PD patients and could be used to improve deep brain stimulation therapy. Deep brain technology already exists but not at the level that Neuralink will hopefully be offering.

Source: Musk’s Neuralink close to clinical trials of “brain interface” device –

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

Keto for PD: The William Curtis Story

Mike Mutzel from High-Intensity Health (author of Belly Fat Effect) talks to William Curtis about his PD journey and how a ketogenic diet changed his life. Curtis suffered from PD for over 17 years before he started exercising, fasting, and following a low-carb, ketogenic diet that remarkably improved his PD symptoms. Through trial and error, Curtis found the right balance in his diet. The William Curtis’ program for easing PD symptoms is not appropriate for everyone. For example, PD patients that have balance problems could do more harm to themselves if they followed Curtis’ diet. After 12 hours of fasting through the night, Curtis has a bulletproof coffee in the morning prepared with butter, heavy cream, coconut oil, and Stevia. This helps his PD symptoms and increases the ketone D-betahydroxybutyrate (BHB).

good results in rats
www.ncbi.nlm.nih.gov/pmc/articles/PMC4912670/

keto vs low fat
8 weeks
both diets had good results, keto was better
pubmed.ncbi.nlm.nih.gov/30098269/

some ways Keto help are not well understood
www.ncbi.nlm.nih.gov/pmc/articles/PMC5790787/

Curtis has a website
ketonesforparkinsons.com/

Could Fasting Help Control PD Symptoms?

This 2019 report in the National Library of Medicine (National Center for Biotechnology Information) looks at lifestyles and dietary habits associated with PD. A fasting mimicking diet (FMD), fasting 3 days followed by 4 days of refeeding for three 1-week cycles, which accelerated the retention of motor function and attenuated the loss of dopaminergic neurons in the substantia nigra in 1-methyl-4-phenyl-1,2,3,6-tetrathydropyridine (MPTP)-induced PD mice. Levels of brain-derived neurotrophic factor (BDNF), known to promote the survival of dopaminergic neurons, were increased in PD mice after FMD, suggesting the involvement of BDNF in FMD-mediated neuroprotection. The findings showed that FMD also inhibited neuroinflammation and modulated the shifts in gut microbiota composition.

Source: Neuroprotection of Fasting Mimicking Diet on MPTP-Induced Parkinson’s Disease Mice via Gut Microbiota and Metabolites – PubMed

Interaction of Mitochondria, a-Syn, and the Endo-lysosomal System

A 2019 study published in the International Journal of Molecular Sciences looked at the interaction of mitochondria, a-synuclein and the endo-lysosomal system. PD is characterized by dopaminergic neuronal loss and the alpha-synuclein-containing Lewy body inclusions in the substantia nigra. Genetic investigations have revealed evidence of the involvement of mitochondrial function, alpha-synuclein (α-syn) aggregation, and the endo-lysosomal system, in disease pathogenesis. Although familial parkinsonism makes up less than 10% of adult parkinsonism, the findings generated from genetic studies have enhanced the understanding of the neuron degeneration processes. These include mitochondrial dysfunction, disruption of network integrity, and α-syn accumulation; the functions of the proteasome and endo-lysosomal pathways in cellular degradation. Mitochondrial dysfunctions, endo-lysosomal disruptions, and α-syn aggregation mutually interact within neurons, while α-syn prion-like propagation may also be associated with PD in an inter-neuronal manner. Both mitochondria and endo-lysosomal dysfunction contribute to the development of α-syn pathology, however, the specific organelle playing the most important role might be decided by genetic and environmental factors. Most likely, a vicious cycle may develop once one system becomes dysfunctional. Further elucidation of the precise molecular mechanisms involved in the pathogenesis of PD may lead to the development of future therapeutic targets to treat PD.

Source: The Overcrowded Crossroads: Mitochondria, Alpha-Synuclein, and the Endo-Lysosomal System Interaction in Parkinson’s Disease

Could α-Synuclein Inhibition be a Treatment for PD?

A 2020 publication in the MDPI journal, Biomolecules looks at targeting a-syn for PD therapeutics. PD is characterized by the loss of dopaminergic neurons in the substantia nigra and the presence of Lewy Bodies (cytoplasmic inclusions). The Lewy Bodies are clumps of protein that can build up and create problems in the brain. The Lewy Bodies contain the aggregated a-synuclein protein that can propagate throughout the brain. Many PD studies have looked at ways of inhibiting a-synuclein accumulation to ease PD symptoms. There are various approaches to a-syn inhibition and multiple clinical trials that examine the link between PD and a-syn, with the hope that a treatment may be found for PD using a-syn. Given the central role of α-syn in PD pathology and progression, α-syn met the criteria to be a tantalizing and evident therapeutic target for PD. Promising strategies include predominantly immunization, anti-aggregative molecules, and an increase in α-syn clearance.

Source: Targeting α-Synuclein for PD Therapeutics: A Pursuit on All Fronts

Ridding Cells of Harmful Protein Aggregates by Inducing Autophagy

This short, enlightening video clip is an extract from a FoundMyFitness interview with Dr. Guido Kroemer. PD is characterized by protein aggregation of a-synuclein and mitochondrial dysfunction, partly due to mitophagy failure. A recently proposed strategy in preventing (or perhaps treating) neurodegenerative diseases like PD is to starve the cells or use biochemical methods to induce general autophagy and thus help the cell rid itself of protein aggregates. Here Dr. Kroemer describes how mitophagy contributes to the pathophysiology of neurodegenerative diseases like PD and Alzheimer’s and how autophagy might mitigate these processes.

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

Can Plant-Based Diets Lower the Risk of Cardiovascular Disease?

A research article published in Plos One in2018 looks at results of multiple observational studies focused on one or more cardio-metabolic risk factors in vegans and omnivorous diets. Macro-nutrient intake and cardio-metabolic risk factors were compared by dietary pattern. People on vegan diets and others on omnivorous diets were compared for energy, saturated fats, body mass index, lipoprotein cholesterol, triglycerides, glucose levels, blood pressure. The results support the idea that plant-based diets are likely to lower the risk of cardiovascular disease and diabetes.

Source: Cardiometabolic Risk Factors in Vegans; a meta-analysis of observational studies

Can Red Yeast Rice be Used to Lower Cholesterol?

An article published by the Penn State Hershey Medical Center looks at red yeast rice (RYR or Went yeast), its use for lowering cholesterol, and the need for further research. RYR acts similarly to statins, particularly monacolin K (Lovastatin). It is not yet determined whether RYR lowers cholesterol because of its statin-like properties or other properties. Studies conducted on RYR support the fact that RYR lowers LDL (“bad”) cholesterol levels. Red yeast (Monascus purpureus) stops the action of an enzyme in the body that helps make cholesterol.  One of the proprietary products most often studied was Cholestin, which contained monacolin. However, current Cholestin products do not contain RYR. Asia, and Chinese communities, use powdered RYR as a food coloring for fish, alcoholic beverages, and cheese. RYR supplements should not be taken by people under 20yrs but for adults, the dosage depends on the formula. Most studies have used 600 mg, 2 to 4 times daily. There are precautions, side effects, and interactions relating to RYR that need to be considered.

Source: Complementary and Alternative Medicine Penn State Hershey Medical Center – Red Yeast Rice

 

Is it Safe to Take CoQ10 While Taking Warfarin or Plavix (clopidogrel)?

Question: Does CoQ10 interact with blood thinners? Answer: There are studies with conflicting results on whether CoQ10 may interfere with warfarin treatment or decrease the effectiveness of warfarin (Coumadin). There are studies that suggest that CoQ10 may increase the risk of bleeding when on warfarin and other studies that suggest CoQ10 may decrease the risk of bleeding when on warfarin. Other studies indicate that there is no effect so long as your INR (bleeding time) is stable. It’s not clear whether CoQ10 affects Plavix treatment. Consult with your doctor before taking any supplement or medication.

Source: ConsumerLab Q&A

Prebiotics to prevent and treat constipation

This 2020 NCBI meta-analysis takes a close look at prebiotics which play a role in augmenting the presence of gut microbiota such as Bifidobacterium, Clostridium, Bacteroidetes, and Lactobacilli which have been demonstrated in functional gastrointestinal disorders. There are only a few studies of the efficacy of prebiotics for chronic constipation and the utility of different commercially available prebiotics in patients with functional and chronic idiopathic constipation. 21 randomized controlled trials were reviewed showing prebiotics to be effective treatments for chronic idiopathic constipation; improvement in stool consistency; the number of bowel moments, and bloating.

Source: Therapeutic Effects of Prebiotics in Constipation: A Review – PubMed

Use of K₂ and Warfarin During Perioperative Period of Catheter Ablation

A study published in the Journal of Pharmaceutical Health Care in 2016 conducted population pharmacokinetic/pharmacodynamic modeling for retrospective clinical data to investigate the effect of vitamin K2on the anticoagulant activity of warfarin in the perioperative period of catheter ablation. 579 INR values of prothrombin time from 100 patients were analyzed using the nonlinear mixed-effects modeling program NONMEM. A 1-compartment model was adapted to the pharmacokinetics of warfarin and vitamin K2, and the indirect response model was used to investigate the relationship between plasma concentration and the pharmacodynamic response of warfarin and vitamin K2.

The population parameters obtained successfully explained the observed INR values and indicated an increase in sensitivity to warfarin in patients with reduced renal function. Vitamin K2 administration of more than 20 mg caused a slight dose-dependent decrease in INR on the day of catheter ablation and a delayed INR elevation after warfarin re-initiation. A pharmacokinetic/pharmacodynamic model was successfully built to explain the retrospective INR data during catheter ablation.

Source: Effect of vitamin K2 on the anticoagulant activity of warfarin during the perioperative period of catheter ablation: Population analysis of retrospective clinical data

What do Studies Say about Probiotics and Digestion?

An article on the Strauss Group website describes probiotic yogurts developed to help regulate digestion and improve symptoms of IBS. The yogurts contain Bifidus Actiregularis bacteria and bio-bacteria. Studies focused on the survival of the bacterium in the gastrointestinal tract and its functionality cover “digestive comfort” a term used to define a well-functioning digestive system without gas, bloating, constipation, etc. The studies specifically relate to the elderly and to women. Probiotics have been shown to help improve brain activity and may be helpful for the nervous system and PD patients. Studies suggest that probiotics may help PD patients by decreasing pro-inflammatory cytokines, oxidative stress, and potentially pathogenic bacterial overgrowth.

Source: Probiotics – Clinical Studies (HE)

Diet and Nutrition as Migraine Triggers

A systematic literature review published on NCBI in July 2020 summarizes evidence from various publications in regard to the role of diet and nutrition as a cause of migraines and as migraine triggers. Data was gathered from primary literature sources from March 2019 to January 2000 in patients over 18 years old. A total of 43 studies were included in the review assessing diet patterns, diet interventions, and diet-related triggers. Among the diets assessed were low-fat, elimination diets, keto diet, and diet-related triggers such as alcohol and caffeine. The review concluded that there is limited high-quality randomized controlled trial data on diet patterns or diet-related triggers. Although many patients already reported avoiding personal diet-related triggers in their migraine management, further research is necessary.

Source: The Role of Diet and Nutrition in Migraine Triggers and Treatments; a systematic literature review

The Migraine-Diet Connection

An article published in the MDPI journal, Nutrients in June 2020 looks at the influence of dietary patterns and dietary triggers on migraines. Identifying these triggers is challenging because so many other factors such as age, genetics, sex, and individual immunological responses to food can influence migraines. If the triggers can be identified they can be avoided to prevent migraines. This review presents the current status of research into diet and migraines and how lifestyle changes may increase the quality of life of patients. The review examines elimination diets; migraine diets; epigenetic diets; the gut-brain axis and probiotics in relation to migraines. The review concludes that the selection of an appropriate diet and obtaining correct dietary counseling is recommended to ensure the biopsychosocial well-being of migraine patients, as strict food avoidance may result in stress and poor quality of life.

Source:Migraine and Diet

What is the Potential of Stem Cell Treatment for PD? (YouTube Webinar)

This webinar is a recording of a live broadcast that took place in June 2019 and consisted of a panel discussion on cell-based therapy for PD. Chairing the panel is Professor Patrik Brundin. The panel of experts includes Gaynor Edwards, a person affected by PD; Parkinson’s neurologist, Clair Henchcliffe and Dr. Roger Barker, consultant neurologist. The panel discusses what kind of stem-cells exist; the source of stem-cells; the uses of stem-cells, and specifically dopamine stem-cells. The panel talks about current trials and the timeline for when stem-cells will be a viable treatment for PD. One of the issues raised is whether we will be able to produce stem-cells in large enough quantities. The panel of experts takes questions from viewers and gives answers on subjects like stem-cell tourist and the cost of treatment. The final word on the subject is that despite the cost of potential stem-cell treatment it will save money spent on the medical care of untreated patients in the long term.