Parkinson's
Episodes
Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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Rhonda Nutrition Parkinson's Microbiome Omega-3 Sulforaphane Sauna Weight Loss Intestinal Permeability CocoaDr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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Rhonda Vitamin D Exercise Brain Alzheimer's Parkinson's Cancer Microbiome Cholesterol Omega-3 Skin Sulforaphane Protein NAD+ Moringa Blood-Brain Barrier CocoaDr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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Rhonda Vitamin D Exercise Parkinson's Epigenetics Omega-3 Fasting Melatonin Vaccine Resveratrol Sauna Insulin COVID-19 Cardiovascular AutoimmunityDr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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How epigenetic predictions align with onset of cancer, Parkinson's and Alzheimer's | Steve Horvath ClipA person's epigenetic age correlates with their risk for developing major diseases of aging like cancer, Alzheimer's disease, and Parkinson's.
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In this clip, Dr. Giselle Petzinger describes her recommended components for an exercise program for people with Parkinson's disease.
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In this clip, Dr. Giselle Petzinger discusses how no evidence exists that lifestyle factors, such as diet and exercise, can cure Parkinson's disease or obviate the need for dopamine replacement.
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In this clip, Dr. Giselle Petzinger discusses how intense exercise can impact motor scores in people with Parkinson's disease.
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Benefits of 1-on-1 therapy & group dynamics in exercise for Parkinson's patients | Giselle Petzinger ClipIn this clip, Dr. Giselle Petzinger explains how to design an optimal exercise regimen for people with Parkinson's disease.
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In this clip, Dr. Giselle Petzinger explains that strenuous exercise affects dopamine sensitivity in the brains of people with Parkinson's disease.
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In this clip, Dr. Giselle Petzinger discusses how adding a cognitive load to an exercise program is important for people with Parkinson's disease.
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In this clip, Dr. Giselle Petzinger discusses the importance of incorporating intensity into the exercise routine for people with Parkinson's disease.
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In this clip, Dr. Giselle Petzinger describes the specific characteristics of exercise that make it so helpful to people with Parkinson's disease.
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In this clip, Dr. Giselle Petzinger describes how exercise may provide a repair model that allows some type of resilience against the insults of Parkinson's disease.
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In this clip, Dr. Giselle Petzinger highlights some of the risk factors for Parkinson's disease, and discusses how this is likely a multifaceted problem.
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How loss of dopamine-producing neurons affects brain circuitry and behavior | Giselle Petzinger ClipIn this clip, Dr. Giselle Petzinger explains how the loss of dopamine disrupts circuitry in the brains of people with Parkinson's disease.
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In this clip, Dr. Giselle Petzinger discusses Parkinson's disease and explains how symptoms can vary dramatically between people.
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Dr. Giselle Petzinger discusses new findings in Parkinson's disease research, emphasizing exercise's role in delaying disease progression.
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Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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Increasing general autophagy as a treatment for neurodegenerative diseases like Parkinson's disease ClipDr. Guido Kroemer describes how mitophagy contributes to the pathophysiology of neurodegenerative disease and how autophagy might mitigate these processes.
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Dr. Gordon Lithgow discusses the roles of protein aggregation, iron overload, and others in the aging process.
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Dr. George Brooks discusses the metabolic pathway known as the “lactate shuttle" and its role in the recovery from traumatic brain injury.
Topic Pages
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Autophagy
Parkinson’s pathology involves impaired PINK1-Parkin–dependent mitophagy, blocking autophagic clearance of damaged mitochondria and α-synuclein aggregates.
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Berberine
Preclinical data indicate berberine mitigates Parkinson's dopaminergic neurodegeneration via AMPK/Nrf2 activation and α-synuclein aggregation suppression.
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Brain-derived neurotrophic factor (BDNF)
Nigral BDNF deficiency diminishes TrkB signaling, weakening dopaminergic neuron survival and accelerating Parkinsonian neurodegeneration.
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Melatonin
Melatonin’s MT1/MT2 receptor signaling and antioxidant actions mitigate dopaminergic oxidative stress and α-synuclein aggregation in Parkinson’s models.
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Small vessel disease
No proven mechanistic link exists; cerebral small vessel disease causes arteriolosclerotic lumen narrowing, chronic hypoperfusion, white-matter infarction.
News & Publications
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Blocking soluble TNF signaling attenuates loss of dopaminergic neurons in models of Parkinson’s disease. (2006) www.sciencedaily.com
Blocking the action of TNF-alpha may slow the progression of Parkinson’s disease.
Parkinson’s disease is a progressive neurodegenerative disorder that affects the central nervous system. It is caused by the destruction of nerve cells in the part of the brain called the substantia nigra. Approximately 1 percent of all adults over the age of 60 years lives with Parkinson’s disease. Findings from a 2006 study suggest that blocking the action of tumor necrosis factor-alpha slows the progression of Parkinson’s disease.
Tumor necrosis factor-alpha (TNF-alpha) is a pro-inflammatory cytokine that is produced by a wide range of cells, including macrophages, lymphocytes, glial cells, and others. TNF-alpha signaling inhibits tumorigenesis, prevents viral replication, and induces fever and apoptosis. Dysregulation of the TNF-alpha signaling pathway has been implicated in a variety of disorders, including cancer, autoimmune diseases, Alzheimer’s disease, and depression.
The investigators injected the brains of mice with either lipopolysaccharide (LPS, an endotoxin that promotes acute inflammation) or 6-hydroxydopamine (a neurotoxin) and assessed the animals' brains for evidence of substantia nigra cell death. They injected a compound called XENP345 (a TNF-alpha inhibitor) into the brains of some of the mice. They also applied LPS and 6-hydroxydopamine to cultured neuronal cells and assessed the effects of XENP345 on cell death.
They found that both LPS and 6-hydroxydopamine caused marked cell death in the substantia nigra region of the animals' brains. They also found that inhibiting TNF-alpha via XENP345 in the brains and in cultured cells reduced cell death by roughly half.
These findings suggest that inhibiting the activity of the pro-inflammatory cytokine TNF-alpha reduces cell death in an animal model of Parkinson’s disease. Robust evidence indicates that exercise, which also reduces inflammation, slows the progression of Parkinson’s disease. Learn more about the effects of exercise on Parkinson’s disease in this episode featuring Dr. Giselle Petzinger.
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SARS-CoV-2 protein drives alpha synuclein aggregation, a hallmark of Parkinson's disease. medicalxpress.com
Scientists have identified an emerging pattern of associations between SARS-CoV-2 (the virus that causes COVID-19) and Parkinson’s disease. For example, the loss of smell is one of the most common symptoms reported in SARS-CoV-2 infection, but it is also an early symptom of Parkinson’s disease, often preceding diagnosis by many years. In addition, some recent case reports describe patients who presented with probable Parkinson’s disease after recovering from severe SARS-CoV-2 infection. Now, evidence from a recent study suggests that the SARS-CoV-2 nucleocapsid protein drives aggregation of alpha synuclein, a hallmark of Parkinson’s disease.
SARS-CoV-2 nucleocapsid proteins are helical structures that are housed within the viral membrane. They encapsulate SARS-CoV-2’s genome, protecting it from the host cellular environment. The virus produces large quantities of nucleocapsid proteins once inside an infected cell because they play critical roles in virion assembly and viral replication.
Alpha synuclein is a type of neuronal protein that regulates synaptic vesicle movements and neurotransmitter release. Its aggregation, a progressive process that spreads from cell to cell, impairing brain function, is a dominant feature in the pathophysiology of Parkinson’s disease.
The authors of the report assessed alpha synuclein aggregation in both the absence and presence of the SARS-CoV-2 spike protein (the virus’s primary infectious particle) and the nucleocapsid protein. They found that in the absence of any SARS-CoV-2 proteins, aggregation naturally occurred after about 10 days. The spike protein had no effect on aggregation time, but following exposure to the nucleocapsid protein, aggregation occurred in less than one day – more than 10 times faster than normal.
Then they studied the effects of the nucleocapsid protein in a cell model of Parkinson’s disease. They injected some of the cells with nucleocapsid protein (about the amount one would expect during SARS-CoV-2 infection) and alpha synuclein and injected some with alpha synuclein alone. They found that twice as many cells injected with both proteins died compared to those injected with alpha synuclein alone.
These findings suggest that the SARS-CoV-2 nucleocapsid protein drives aggregation of alpha synuclein and promotes cells death in a model of Parkinson’s disease. Learn more about Parkinson’s disease in this episode featuring Dr. Gizelle Petzinger.
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Nanoparticles in air pollution accumulate in the brains of young adults: A common denominator in neurodegenerative disease? www.sciencedaily.com
Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the two most common neurodegenerative conditions in older adults, affecting a combined 36 million people worldwide. Evidence suggests that exposure to air pollution increases the risk of developing these diseases. Findings from a recent study demonstrate that particulate matter in air pollution accumulates in the brains of young adults and may serve as a common denominator in the pathophysiology of AD and PD.
Particulate matter in air pollution is a mixture of solid particles and liquid droplets. It is present in fine inhalable particles, with diameters that are generally 2.5 micrograms or less. Ultrafine particles less than 1 microgram in diameter, referred to as nanoparticles, are often enriched in highly reactive metals such as iron, aluminum, titanium, and others. They may serve as catalysts for reactive oxygen species formation and promote protein misfolding and aggregation. Nanoparticles in air pollution are not regulated and carry many health risks. They are also present in food additives and food packaging materials.
The authors of the study documented biomarkers of AD and PD present in brainstem samples taken during the autopsies of 186 healthy children and young adults (age range, 11 months to 27 years) living in the metro area of Mexico City, a region known for its high levels of air pollution. They also conducted magnetic remanence studies to quantify the presence of metal-rich nanoparticles in the brainstem samples. Finally, using high resolution scanning and transmission electron microscopy and energy-dispersive X ray analysis, they identified the composition, location, size, and shape of nanoparticles in the substantia nigra region of a randomly chosen single sample taken from the larger group. Damage to the substantia nigra is a hallmark of PD.
They found that all of the brainstem samples contained iron-, aluminum-, and titanium-rich nanoparticles. The quantity of nanoparticles varied among the brain samples, likely due to the level and duration of exposure. The authors posited that these nanoparticles could have been acquired via both oral and respiratory routes from food sources and airborne exposures, respectively. Damage to the mitochondria, endoplasmic reticulum, and neuromelanin in the single brainstem sample correlated with the presence of iron-, aluminum-, and titanium-rich nanoparticles.
These findings suggest that exposure to nanoparticles is pervasive, with evidence confirmed as early as 11 months of age. Such exposures may put people living in urban areas where high levels of air pollutants are present at greater risk for developing AD and PD.
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BDNF mimetic 7,8-dihydroxyflavone protects neurons against cell death. www.sciencedaily.com
BDNF’s neuroprotective capacity suggests that it could be useful in preventing or treating neurodegenerative diseases. Circumventing problems with BDNF’s delivery, half-life, and other limitations has proven challenging. A 2010 study found that 7,8-dihydroxyflavone, a BDNF mimetic, exerted neuroprotective qualities similar to those of BDNF.
7,8-dihydroxyflavone is a type of flavonoid compound present in a variety of plants. Flavonoids exert antioxidant and anti-inflammatory effects, among others. Some evidence indicates that 7,8-dihydroxyflavone might be useful in reversing the damage associated with lead poisoning in children.
The authors of the study screened 2,000 bioactive compounds to gauge their ability to protect rodent and human neurons from apoptosis and identified five compounds, including 7,8-dihydroxyflavone, that showed potential in protecting the cells. Then they treated the cells with BDNF and the various compounds and deprived the cells of oxygen and glucose.
They found that none of the compounds was as effective as 7,8-dihydroxyflavone in protecting the cells from apoptosis. In fact, 7,8-dihydroxyflavone was even more protective than BDNF. They also found that 7,8-dihydroxyflavone exerted its protective qualities by activating a receptor called TrkB, to which BDNF binds. They replicated their findings in an in vivo study of mice, indicating that 7,8-dihydroxyflavone enhances neuronal survival.
These findings demonstrate that flavonoid compounds that mimic the effects of BDNF show potential as therapeutics against neurodegenerative diseases.