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Treatments for Sleep Changes

Treatments for Sleep Changes

Individuals suffering from Alzheimer’s disease frequently struggle to fall asleep or may notice alterations in their sleep routine. Researchers are still unsure of the exact cause of these sleep disruptions. Similar to modifications in behavior and memory, sleep abnormalities are inextricably linked to the brain damage caused by Alzheimer’s disease. It is always best to try non-drug coping mechanisms first when handling sleep changes.

Common sleep changes
Sleep patterns are altered in a large number of Alzheimer’s patients. The reason why this occurs is not fully understood by scientists. Similar to alterations in behavior and memory, sleep abnormalities are inextricably linked to the brain damage caused by Alzheimer’s disease. Sleep disturbances are also common in older adults without dementia, but they tend to be more severe and occur more frequently in those with Alzheimer’s. While some studies have found sleep abnormalities in the early stages of the disease, there is evidence that they are more common in later stages.


Sleep changes in Alzheimer’s may include: the inability to sleep. Many who have Alzheimer’s disease wake up more frequently and remain awake through the night more often. Reduces in dreaming and non-dreaming stages of sleep are observed in brain wave studies. People with trouble falling asleep may wander, be unable to stay still, or scream or call out, which can keep their carers awake. naps during the day and other changes to the sleep-wake cycle. People may experience extreme daytime sleepiness followed by difficulty falling asleep at night. In the late afternoon or early evening, they might become agitated or restless, a phenomenon known as “sundowning.”.

According to expert estimates, people with advanced Alzheimer’s disease sleep a large portion of the day and spend approximately 40% of the night awake in bed. Extreme situations may cause a person’s typical pattern of daytime wakefulness and nighttime sleep to completely reverse.

Contributing medical factors
A comprehensive medical examination should be performed on anyone having trouble sleeping to rule out any curable conditions that might be causing the issue. Depression, restless legs syndrome, which causes unpleasant “crawling” or “tingling” sensations in the legs and an overwhelming urge to move them, and sleep apnea, which is an abnormal breathing pattern in which people briefly stop breathing many times a night, leading to poor sleep quality, are a few conditions that can exacerbate sleep problems. Treatment options for sleep disorders primarily caused by Alzheimer’s disease include both non-drug and drug approaches.

The National Institutes of Health (NIH) and the majority of experts strongly advise against using medication in favor of non-drug measures. Research has indicated that the general quality of older adults’ sleep is not enhanced by sleep medications. The risks of using sleep aids include an increased risk of falls and other problems that might offset any therapeutic advantages.

Non-drug treatments for sleep changes
Non-pharmacological therapies seek to lessen midday naps and enhance sleep hygiene and routine. It is always advisable to try non-drug coping strategies before taking medication because some sleep aids have serious side effects. Maintaining regular mealtimes, bedtimes, and wake-up times, seeking morning sunlight exposure, and regularly scheduled exercise, but no later than four hours before bedtime, avoiding alcohol, caffeine, and nicotine, treating any pain, making sure the bedroom temperature is comfortable, providing nightlights and security objects, discouraging the person from staying in bed while awake, and encouraging them to use the bed only for sleep, are all important ways to create a welcoming sleeping environment and promote rest for someone with Alzheimer’s disease.

Medications for sleep changes
Sometimes non-drug treatments don’t work as planned, or the sleep disruptions are accompanied by unruly behavior at night. Experts advise that treatment for those who do need medication “begin low and go slow.”. Using sleep aids when an older person has cognitive impairment carries a significant risk. These include a heightened risk of fractures and falls, disorientation, and a deterioration in self-care skills. When a regular sleep pattern has been established, an attempt should be made to stop using sleep medications.

The kinds of behaviors that may accompany sleep changes can have a significant impact on the type of medication that a doctor prescribes. Using an antipsychotic medication should only be decided very carefully. Studies have indicated that these medications raise the risk of stroke and death in elderly dementia patients. The U.S. S. The Food and Drug Administration (FDA) has mandated that manufacturers label these medications with a disclaimer that states they are not authorized to treat symptoms of dementia and a “black box” warning about potential risks.

Reference:

https://www.alz.org/alzheimers-dementia/treatments/for-sleep-changes
https://www.mayoclinic.org/healthy-lifestyle/caregivers/in-depth/alzheimers/art-20047832
https://www.sciencedirect.com/science/article/pii/S0197457218300466
https://www.mcmasteroptimalaging.org/blog/detail/blog/2023/08/17/non-drug-options-for-dementia-related-sleep-problems

Medications that have been suggested by doctors worldwide are available here
https://mygenericpharmacy.com/category/disease/alzheimer-disease

Ozempic-like drug may help slow the progression of Parkinson’s symptoms

Ozempic-like drug may help slow the progression of Parkinson’s symptoms

Scientists have found that a drug commonly used to treat type 2 diabetes can help reduce the development of motor skills deterioration in people with early-stage Parkinson’s, according to the findings of a new study published in The New England Journal of Medicine. The study, which was randomized, double-blind, and placebo-controlled, followed 156 participants in France whose diagnosis of Parkinson’s had been within the last three years, were on a stable regime of medication to treat symptoms, and who did not yet have marked decline in motor skills. The participants were either given lixisenatide, a GLP-1 receptor agonist that is used to treat diabetes, or a placebo.

After 12 months, the 78 people who had been given lixisenatide showed virtually no further deterioration of motor skills that is commonly seen with Parkinson’s disease, while those who were given a placebo saw a worsening of those symptoms. Nearly half of the group who took lixisenatide reported nausea and 13% experienced vomiting. It is a fascinating study that is proof of concept that this class of medications may have some protective effect and be of advantage to someday treat Parkinson’s. It will be interesting to see if the results hold true for other newer GLP-1 agents like Ozempic/Wegovy and Zepbound, Gabbay said.

Parkinson’s is a disorder characterized by significant neurological decline that can manifest in tremors, motor control problems, and dementia. There is no known cause, but it is associated with a lack of dopamine in the brain. It is the second most common neurological disease after Alzheimer’s in the U.S., and it is believed that at least 500,000 adults in the U.S. have it.

Daniel Truong, MD, neurologist and medical director of the Truong Neuroscience Institute at MemorialCare Orange Coast Medical Center in Fountain Valley, CA, and editor-in-chief of the Journal of Clinical Parkinsonism and Related Disorders, told MNT that links between Parkinson’s and diabetes hinge on several common threads between the disorders: There is ongoing research exploring the potential links between diabetes and Parkinson’s disease. Several studies have suggested that individuals with diabetes may have a higher risk of developing Parkinson’s disease, and vice versa, Truong said.

Chronic low-grade inflammation and oxidative stress are common features of both diabetes and Parkinson’s disease. Research suggests that inflammatory processes in the brain may play a role in the progression of Parkinson’s disease, and there is evidence linking inflammation to insulin resistance in diabetes. Studies have shown that mitochondrial dysfunction contributes to insulin resistance and beta-cell dysfunction in diabetes, while mitochondrial impairment is also a key feature of dopaminergic neuron degeneration in Parkinson’s disease.

Emerging evidence suggests that alpha-synuclein pathology may also be present in peripheral tissues, including pancreatic beta cells in individuals with diabetes. Further research could explore the role of alpha-synuclein aggregation in diabetes-related complications and its potential link to Parkinson’s disease. GLP-1 (glucagon-like peptide-1) receptor agonists are part of a treatment regimen for people with type 2 diabetes. They can help reproduce or enhance the effects of a naturally occurring gut hormone that assists in the control of blood sugar levels, and they can also reduce appetite by working on brain hunger centers; this is one of the reasons drugs like Ozempic and Wegovy have been associated with weight loss.

Truong said that a drug like lixisenatide has neuroprotective effects, which would clearly provide some assistance for people with a neurological disorder like Parkinson’s. But he also pointed out how common traits in both diabetes and Parkinson’s can provide some insight into GLP-1 receptor agonists as a way to reduce Parkinson’s symptoms.

There is emerging evidence suggesting shared pathophysiological mechanisms between diabetes and Parkinson’s disease. For example, insulin resistance and impaired glucose metabolism have been implicated in both conditions. Therefore, drugs that target these mechanisms, such as GLP-1 RAs, might have beneficial effects in both diseases.
In some studies, the prevalence of Parkinson’s disease was lower among patients with diabetes who were treated with glucagon-like peptide-1 (GLP-1) receptor agonists or dipeptidyl peptidase-4 inhibitors, which increase GLP-1 levels, than among patients who received other diabetes medications.

Truong said that the study’s limitations warrant further research to establish several aspects of long-term treatment of Parkinson’s with GLP-1 receptor agonists: dose optimization, combination therapies, safety and tolerability, and effects on the non-motor symptoms. Parkinson’s disease is associated with a wide range of non-motor symptoms, including cognitive impairment, autonomic dysfunction, and psychiatric symptoms. Future studies should investigate whether lixisenatide has beneficial effects on non-motor symptoms in addition to motor symptoms.

Although the study suggested a potential neuroprotective effect of lixisenatide, the underlying mechanisms are not fully understood. Further research is needed to elucidate the specific neuroprotective mechanisms of lixisenatide in Parkinson’s disease, including its effects on inflammation, oxidative stress, mitochondrial function, and alpha-synuclein pathology.

REFERENCES:
https://people.com/ozempic-like-drug-slowed-progression-parkinsons-disease-new-trial-8627473
https://www.medicalnewstoday.com/articles/ozempic-like-drug-may-help-slow-progression-parkinsons-symptoms
https://www.cnbc.com/2024/04/04/drug-similar-to-ozempic-slowed-parkinsons-disease-in-small-trial.html

Medications that have been suggested by doctors worldwide are available here
https://mygenericpharmacy.com/index.php?cPath=1_22_846

The Relationship Between Pesticides and Parkinson’s

The Relationship Between Pesticides and Parkinson’s

A discussion of how environmental factors, such as pesticides, may affect your risk of Parkinson’s disease. During my recent interview on Wisconsin Public Radio, many of the callers asked questions related to the environmental risks of Parkinson’s disease (PD), specifically, exposures related to farming. Those calls prompted me to delve further into this complicated and murky topic. Before we start discussing specific factors in the environment that may increase the risk of PD, let’s understand some basic ground rules that will help put this topic in perspective person’s genetic makeup is likely more important in determining whether he or she develops PD than any environmental risk factor. This is probably the case even in a person without a known family history of PD. However, environmental exposure may be important in triggering the disease in a person genetically susceptible to it.
It is important to note that any particular environmental exposure that we will talk about, typically increases the risk of PD by a very small amount. The risk will also depend on dosage and frequency of exposure, which means that a small and/or infrequent exposure may have a very small impact on PD risk.

Certain chemical exposures, like coffee or non-steroidal anti-inflammatory drugs, seem to lower the risk of Parkinson’s disease (PD). All of the variables that can raise or lower a person’s risk for Parkinson’s disease must be considered to fully determine their risk. There are probably other chemicals in our environment that affect the risk of Parkinson’s disease (PD) as well. These chemicals are not yet well studied, so I won’t discuss them here. Being in a modern society exposes us to a wide range of chemicals, the risks of which we are not fully aware. Given this context, let’s get started. Research from the 1980s indicated that early exposure to a rural environment and well water was linked to the development of Parkinson’s disease (PD) in later life. These questions were then the subject of numerous more investigations. Although the results of the studies are inconsistent, overall the evidence points to links between each of the following factors and an increased risk of Parkinson’s disease: drinking well water, living in a rural area, working as a farmer, exposure to farm animals, and living on a farm.

Naturally, there is a connection between all of these categories because farmers use pesticides, drink well water, and are more likely than urban residents to live on farms in rural areas where they are also exposed to farm animals. The goal of the studies was to determine why living in a rural area raised the risk of Parkinson’s disease. Is there a higher risk for people who live on farms, or is it just a part of living there? Is it because of pesticide exposure, well water exposure, animal exposure, or something else related to living in a rural area?

Ultimately, the claim that each of these factors raises the risk of Parkinson’s disease is supported by epidemiologic data. It should be noted that all of the elevated risks in these studies are negligible, typically 1-2 times higher than the risk in the general population. A recent study attempted to revisit this issue because farming life has changed since the majority of studies regarding Parkinson’s disease and rural living were conducted decades ago. There is less reliance on well water in rural communities, there has been a significant migration from rural to urban areas, and there is a decrease in the use of pesticides. The incidence of Parkinson’s disease (PD) in rural versus urban areas was examined in a recent study that was done in Finland. Curiously, being a rural resident is still associated with PD risk. Probably, the environmental exposures from decades ago are still reflected in the diagnoses of Parkinson’s disease (PD), and future research may reveal additional benefits from risk reduction in rural areas brought about by a decline in pesticide use and other farming-related changes. However, the study raises the possibility that our knowledge of the relationship between Parkinson’s risk and rural living is still incomplete.

Since data on this topic is often collected in large populations, it raises the question of which specific pesticides are most concerning given the evidence linking pesticide use to an increased risk of Parkinson’s disease (PD). Frequently, study participants are unaware of the precise pesticide exposures they have had. This makes figuring out which pesticides to stay away from challenging. However, some research was able to look into the dangers of particular substances. The most recent review summed up what is currently known about this subject. Paraquat has the most data connecting it to an elevated risk of Parkinson’s disease (PD); exposure to it is linked to a 2-3-fold increased risk of PD over the general population. A very thorough study looked at the relationship between the risk of Parkinson’s disease and exposure to thirty-one pesticides. The two pesticides that should worry people the most, according to the data, are rotenone and paraquat. Reactive oxygen species are intracellular chemicals that produce oxidative stress and cause cell damage. This is how paraquat works. The way rotenone works is by causing damage to the mitochondria, which are responsible for producing energy necessary for cell survival. It’s interesting to note that oxidative stress and mitochondrial dysfunction are prevalent themes in our understanding of what ultimately leads to nerve cell death in Parkinson’s disease.

Several pesticides have been associated with an increased risk of Parkinson’s disease, including:

  1. Paraquat: This herbicide has been strongly linked to an increased risk of Parkinson’s disease. Exposure to paraquat has been shown to induce oxidative stress and damage dopaminergic neurons, which are the cells primarily affected in Parkinson’s disease.
  2. Rotenone: Another pesticide, rotenone, has also been implicated in the development of Parkinson’s disease. Rotenone works by inhibiting mitochondrial function and increasing oxidative stress, leading to neuronal damage similar to that seen in Parkinson’s disease.
  3. Organochlorine pesticides: Some studies have suggested a potential link between exposure to organochlorine pesticides, such as dieldrin and lindane, and an increased risk of Parkinson’s disease. These pesticides have been shown to accumulate in the brain and may contribute to neurodegeneration.
  4. Organophosphate pesticides: Exposure to certain organophosphate pesticides, such as chlorpyrifos and diazinon, has also been associated with an increased risk of Parkinson’s disease. Organophosphates can interfere with neurotransmitter function and may contribute to the development of Parkinson’s disease through various mechanisms.

It’s important to note that while these pesticides have been associated with an increased risk of Parkinson’s disease, not everyone exposed to them will develop the condition. Parkinson’s disease is likely influenced by a combination of genetic and environmental factors, and pesticide exposure may represent one piece of the puzzle. Additionally, more research is needed to fully understand the relationship between pesticide exposure and Parkinson’s disease.

REFERENCES:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5683846/
https://www.thelancet.com/journals/lanplh/article/PIIS2542-5196(23)00255-3/fulltext#section-3d6acba1-acea-4be2-8dc9-b7e14e5b6583
https://www.apdaparkinson.org/article/the-relationship-between-pesticides-and-parkinsons/

Medications that have been suggested by doctors worldwide are available here
https://mygenericpharmacy.com/index.php?cPath=1_22_846

B3 vitamin form may aid in the treatment of Parkinson’s disease.

B3 vitamin form may aid in the treatment of Parkinson’s disease.

Over 10 million individuals worldwide suffer from Parkinson’s disease. For now, there is no treatment for Parkinson’s disease. Nicotinamide adenine dinucleotide (NAD+), an energy molecule, has been the subject of research for a few years as a potential treatment for the illness. A high dose of NR, a form of vitamin B3, has been shown in a phase 1 clinical trial to help raise NAD+ levels in Parkinson’s disease patients. Parkinson’s disease clinical symptom improvement may be linked to NR supplementation. According to research, Parkinson’s disease affects over 10 million people worldwide, making it the second most common neurodegenerative illness after Alzheimer’s. For now, there is no treatment for Parkinson’s disease. Through the various stages of the disease, symptoms are managed with medication, lifestyle modifications, and occasionally surgery. In recent years, scientists have also investigated nicotinamide adenine dinucleotide (NAD+), a crucial molecule that aids in the body’s energy production, as a potential Parkinson’s disease treatment.

Previous studies indicate that NAD+ deficiency may be present in Parkinson’s patients, and raising NAD+ levels may be beneficial. According to a phase 1 clinical trial, giving patients with Parkinson’s disease high dose supplements of nicotinamide riboside (NR), a precursor to NAD+ and a source of vitamin B3, increased their whole blood NAD+ levels and expanded their NAD+ metabolome. These findings may be linked to a reduction in their clinical symptoms. It is still early in the research process, so it cannot be definitively established that supplementing with NR will alleviate Parkinson’s disease symptoms. The journal Nature Communications published the study not too long ago. As stated by Prof. “NR is a form of vitamin B3 and a precursor of NAD+,” says co-lead author Charalampos Tzoulis, a professor of neurology and neurogenetics at the University of Bergen and Haukeland University Hospital, Bergen, Norway. According to Dr. Tzoulis, who spoke with Medical News Today, NAD+ is a necessary coenzyme that is involved in a number of biological functions, such as DNA repair, regulation of gene expression, and mitochondrial function—the cell’s powerhouses that handle energy.

He continued, “Research has demonstrated that aberrant energy metabolism, resulting from dysfunction in the mitochondria, occurs in the brain of individuals with Parkinson’s disease and is thought to contribute to the onset and advancement of the disease.”. Dr. NAD+ levels typically decrease with age, according to Daniel Truong, a neurologist who is the medical director of the Truong Neuroscience Institute at MemorialCare Orange Coast Medical Center in Fountain Valley, California, and the editor-in-chief of the Journal of Clinical Parkinsonism and Related Disorders. Truong was not involved in this study. According to Dr. Truong, energy metabolism, mitochondrial function, anti-aging, and DNA repair are a few possible applications and advantages of NR. According to certain studies, NR may have neuroprotective qualities. The ChromaDex External Research Program (CERPTM) funded this study by donating Niagen®, a patented NR ingredient from ChromaDex, to further the research.

Twenty people with idiopathic Parkinson’s disease participated in the phase 1 clinical trial. Over four weeks, participants were given a daily dose of either 3,000 mg of NR in the form of an oral supplement or a placebo. Following that, an ECG, clinical and molecular measurements, and the MDS-UPDRS rating scale were used to evaluate study participants’ degree of Parkinson’s disease symptoms. Compared to patients who received a placebo, researchers observed that NR significantly raised NAD+ levels and altered the NAD+ metabolome in whole blood. The Movement Disorder Society Unified Parkinson’s Disease Rating Scale (MDS-UPDRS) was used to measure clinical symptoms of Parkinson’s disease, and the study’s findings indicate that high-dose NR was both safe and well-tolerated by study participants. These findings suggest that increasing NAD+ levels may have a symptomatic anti-Parkinson’s effect. According to Dr. Tzoulis, the study demonstrated that a high dose of NR 3 gr [grams] per day of treatment is safe for a month when used short-term and could therefore be investigated in longer-term clinical trials. It is important to emphasize that our study does not prove that this NR dose is generally safe or that taking it for longer than 30 days is safe. Longer-term research is still needed to determine this.

Furthermore, he added, the study demonstrated that taking NR 3 gr daily causes a significant rise in blood NAD levels and associated metabolites without having any negative metabolic effects after 30 days. He did, however, issue a warning, stating that even though the study found a slight clinical improvement linked to NR treatment, this cannot be taken to indicate a clinical effect because the purpose of the study was not to find a clinical improvement. This study’s primary goal was to ascertain the 3,000 mg NR daily’s short-term safety. We must investigate higher-dose regimens in order to fully utilize NR’s therapeutic potential, according to Dr. Tzoulis. The short-term safety of 3,000 mg NR daily is established by this study, opening the door for future therapeutic trials to investigate high-dose options. He continued, “We look forward to the results from our year-long NO-PARK phase 2/3 study on 400 persons with Parkinson’s disease, which is already ongoing at our Center and estimated to conclude by the end of 2024, as conclusive proof on the therapeutic potential of NR in Parkinson’s disease.”. You can view public information about the NO-PARK study at clinicaltrials.gov and neuro-sysmed.com.

Movement disorders neurologist Dr. Rocco DiPaola of the Hackensack Meridian Neuroscience Institute at Jersey Shore University Medical Center told MNT that after reading this study, his initial impression is that it offers a possible treatment that might help slow the progression of Parkinson’s disease. Neuroprotection is a treatment that may help avoid some of the long-term complications associated with advancing disease, but there [are] currently no treatments that offer this. To prove safety, the current study was conducted on a small scale and for a brief period of time. It would take a large-scale trial with [a] longer treatment duration to confirm safety and a neuroprotective benefit. Dr. Truong concurred, pointing out that while the results are encouraging, larger, longer-term trials—especially double-blind ones—are necessary to duplicate and build upon this one study’s findings. He went on, “I find the study’s suggested mechanism of action, which involves raising NAD+ levels and possibly having neuroprotective effects, to be quite intriguing.”. They would like to know how this could be incorporated, taking patient tolerance and safety profile into account, into the current Parkinson’s disease treatment protocols. Dr. Truong continued, “Any possible new therapeutic avenue is of interest given the current status of treating Parkinson’s disease.”. Particularly alluring is the notion of a supplement that might lessen clinical symptoms and even stop the course of the illness.

REFERENCES:

https://www.parkinsons.org.uk/news/more-research-shows-potential-benefits-vitamin-b3-parkinsons
https://www.medicalnewstoday.com/articles/nr-vitamin-b3-parkinsons-disease-symptoms-study
https://www.parkinsons.org.uk/news/vitamin-b3-supplement-shows-early-promise-parkinsons
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8245760/

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Parkinson’s disease and dementia may have an impact on the brain due to nanoplastics.

Parkinson’s disease and dementia may have an impact on the brain due to nanoplastics.

Scientists at Duke University School of Medicine have discovered that nanoplastics alter a particular protein in the brain, which results in alterations connected to dementias other than Parkinson’s. Worldwide, Parkinson’s disease affects more than 10 million individuals. Scientists are aware that a person’s lifestyle, genetics, and environment all contribute to the development of disease. Researchers at Duke University School of Medicine discovered that a particular protein in the brain is impacted by nanoplastics, which are minuscule plastic particles that break down in the environment and can seep into soil and water. These changes have been connected to Parkinson’s disease and other forms of dementia. Science Advances, a journal, published the study recently. Parkinson’s disease is thought to be the neurological ailment with the fastest global growth rate. According to research, the condition affects over 10 million people worldwide. For now, there is no treatment for Parkinson’s disease. Although the exact cause of the illness is still unknown, scientists do know that genetics, lifestyle choices, and environmental factors all have an impact.

Parkinson’s disease is not usually heritable or transmissible, according to Dr. Andrew West, professor in the Department of Pharmacology and Cancer Biology at Duke University School of Medicine and the study’s principal investigator. Environmental exposure to toxins and pesticides is thought to be a contributing factor in the disease’s risk. Dr. West told Medical News Today, However, the known environmental risks account for a very small percentage of what may be lurking out there, increasing our risk of getting sick. Once we have determined that there is a real risk of disease or that the disease will progress due to environmental factors, we can take precautions to reduce that risk. Mr. According to West, he and his colleagues first used various kinds of nanoparticles to help with biomarker assays for dementia and Parkinson’s disease diagnosis. By coincidence, they discovered that a protein called alpha-synuclein, which has been connected to brain disorders, could be greatly inhibited by some forms of nanoparticles.

In this study, three test tube models, cultured neurons, and a Parkinson’s disease-modeling mouse were utilized by the researchers. Dr. West and his colleagues discovered that the alpha-synuclein protein is drawn to and accumulates in response to nanoparticles of the plastic polystyrene used to make foam packing peanuts, egg cartons, and disposable drinking cups. Dr. West said, We discovered through various assays that nanoplastics may sever portions of the alpha-synuclein protein, which typically binds to lipids in the brain, and twist the protein into a form that may encourage aggregation associated with disease.. But the issues don’t end there; the plastics may also damage the machinery that is meant to break down aggregates, which are part of the lysosome, a component of the cell. Dr. West continued, We believe the interactions we observed in the model are driven by this ‘two-hit’ mechanism.

Microplastics are the first tiny particles formed when plastic degrades in the environment. After that, the microplastics keep breaking down to create new ones. According to a March 2022 study, people’s gastrointestinal tracts absorb roughly 5 grams of microplastic and nanoplastic per week on average. The general health of an individual may be harmed by both microplastics and nanoplastics, according to earlier research. For instance, studies have shown that nanoplastics may be connected to specific cancer types and can also interfere with the normal functions of lung and liver cells. Furthermore, there has previously been research on the connection between brain health and nanoplastics. According to studies that were released in June 2020, the brain can be adversely affected by micro- and nanoplastic exposure, which increases the risk of neuronal disorders. According to a study that was released in April 2023, mice that consumed nanoplastics had lower short-term memory and cognitive function.

According to Dr. West, these findings strongly suggest that technology should be developed to track the build-up of plastic pollution in the human brain and to track the susceptibility of various individuals to Parkinson’s disease and other neurological disorders based on their individual exposures. We could create laws and technological solutions to ensure that harmful nanoplastic actors stay out of our food and water if we understood the precise molecular makeup of these individuals. As for the research’s next steps, Dr. West stated that they hope to conduct longer-term studies using chronic dosing to find out how various nanoplastic kinds impact various molecular processes that are thought to be responsible for disease risk and progression. In order to make our lab models more informative, he continued, we also need to have a better idea of what lifetime exposures to different types of nanoplastics look like.. MNT also discussed this study with Dr. Rocco DiPaola, a neurologist who oversees the Movement Disorder Program at Jersey Shore University Medical Center’s Hackensack Meridian Neuroscience Institute.

According to Dr. DiPaola, this study could add to our understanding of the mechanisms underlying Parkinson’s disease and other disorders linked to alpha-synuclein. It has long been believed that a major contributing factor to the development of these disorders is a combination of genetic factors and an environmental trigger. It is an additional possible cause of these illnesses. When asked how readers can protect themselves from environmental factors that may increase their risk for Parkinson’s disease and other types of dementia, Dr. DiPaola said that while there is no way to mitigate all risks, limiting exposure to toxins, such as pesticides, would be one way to limit risk. Environmental factors are likely one of many factors that play a major role in the development of Parkinson’s disease. He continued, Previous environmental studies have found increased risk with exposure to well water, growing up in a rural area, and pesticide exposure.

REFERENCES:

https://www.medicalnewstoday.com/articles/parkinsons-dementia-how-nanoplatics-affect-protein-in-brain#More-insights-into-what-may-cause-neurodegenerative-diseases
https://www.news-medical.net/news/20231117/Study-links-nanoplastics-to-Parkinsons-disease-and-dementia.aspx
https://www.sciencedaily.com/releases/2023/11/231117181023.htm
https://www.science.org/doi/10.1126/sciadv.adi8716

For parkinsons disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_293

Tai chi help slow the progression of Parkinson’s

Tai chi help slow the progression of Parkinson’s

According to a recent study, tai chi may benefit Parkinson’s disease sufferers. Parkinson’s disease has no known cure, and although current treatments reduce symptoms, they don’t seem to stop the disease’s progression. Parkinson’s disease patients can benefit from physical treatment that teaches their brains to compensate for lost mobility. This helps improve their gait and balance. According to recent studies, practicing tai chi, a Chinese martial art that entails a sequence of slow motions and postures, may help reduce Parkinson’s disease symptoms and decrease the disease’s progression.

The research, which was published on October 24 in the Journal of Neurology, Neurosurgery & Psychiatry, discovered that tai chi practitioners with Parkinson’s disease experienced a slower deterioration in cognitive function than non-practitioners. Parkinson’s disease has no known cure, and although current treatments reduce symptoms, they don’t seem to stop the disease’s progression. According to the researchers, regular exercise, such as tai chi, may help manage symptoms and slow the disease’s progression. Dr. Molly Cincotta, a neurologist at Temple University Hospital and assistant professor of clinical neurology at Temple University’s Lewis Katz School of Medicine, claims that previous research indicates exercise is one of the only interventions that appears to reduce the progression of Parkinson’s disease. Parkinson’s patients’ gait and balance can also be enhanced by physical treatment that teaches brain regions to compensate for lost movement.

Beginning in January 2016, researchers recruited 330 Parkinson’s disease patients to learn how tai chi affects the disease’s symptoms and complications. For the study, the average observation period was 4.3 years. The participants were divided into two groups: 143 engaged in one-hour, twice-weekly tai chi practice, and 187 got normal medical care without engaging in any tai chi exercises. All patients had their disease progression evaluated by the research team at the beginning of the study, and then again in November 2019, October 2020, and June 2021. They examined the degree of mobility, mood, sleep quality, and cognitive abilities of the subjects as well as the autonomic nervous system’s performance (including bowel and urine movements).

The group who practiced tai chi showed slower illness progression, according to the team’s findings. Tai chi practitioners reported better sleep, balance, and cognitive function as well as fewer difficulties. For instance, compared to 7.5% of individuals who did not practice tai chi, 1.4% of those in the tai chi group exhibited dyskinesia. Moreover, mild cognitive impairment (MCI) was observed in 2.8% of tai chi practitioners as opposed to 9.6% in the non-tai chi group. Additionally, those who did not practice tai chi used more medications. Compared to 71% of those who consistently practiced Tai Chi, over 83% of people who did not practice the art needed to increase their prescription in 2019. Compared to 87% of individuals who practiced tai chi, over 96% of those who did not practice the kind of meditation required a higher dosage in 2020.

“In patients with idiopathic Parkinson’s disease, this study suggests that regular [tai chi] practice may be beneficial for motor function, sleep, cognition, and overall quality of life,” stated Cincotta. Parkinson’s disease is a neurodegenerative condition primarily marked by the death of brain cells that generate dopamine, a neurotransmitter essential for mood regulation, thought processes, and motor function, among other bodily processes. It’s like trying to drive with the parking brake on when these cells are gone and the brain has less dopamine. Although movement is possible, it is frequently jerky, stiff, and slow, according to Cincotta. According to Cincotta, a deficiency in dopamine can eventually result in tremors, changed facial expressions, a shuffling gait, anxiety, despair, or indifference.

Increased inflammation may also be a result of the disease, and research indicates that the more inflammatory chemicals the body produces, the more severe the symptoms usually are. The primary treatment for Parkinson’s disease is medication. These medications, which work by increasing low dopamine levels, alleviate symptoms but don’t seem to have a major effect on the course of the illness. Furthermore, some medications may become less effective as the illness progresses.

The University of Miami Health System’s chief of the Division of Movement Disorders, Dr. Ihtsham ul Haq, asserts that the only approach to delay the progression of Parkinson’s disease is through exercise. He stated, “Tai chi is a great way to get this benefit, but it’s definitely not the only way.” Scientists are trying to figure out why exercise affects Parkinson’s disease in this way. According to Haq, frequent exercise may alter cellular processes including protein aggregation and mitochondrial function, as well as enhance cardiovascular health and reduce inflammation. Cincotta continued, “Tai chi in particular may support people in maintaining their social connections, which has a positive effect on cognition.”

Haq asserts that it’s difficult to say whether one form of exercise is superior than another. People with Parkinson’s disease should exercise in any way they find rewarding as often as it is convenient for them, according to Haq, as no limit has been identified to the effect. According to recent studies, tai chi may lessen Parkinson’s disease symptoms and delay the disease’s progression. Parkinson’s disease is mostly treated with medication; however, the medications now on the market don’t seem to slow the disease’s progression. Numerous studies indicate that the only intervention that appears to be effective in delaying the course of disease is exercise, such as tai chi.

REFERENCES:

https://lifestyle.livemint.com/health/wellness/tai-chi-parkinsons-symptoms-physical-activity-111698644544772.html
https://www.medicalnewstoday.com/articles/can-tai-chi-help-slow-the-progression-of-parkinsons
https://www.healthline.com/health-news/tai-chi-may-help-alleviate-some-symptoms-of-parkinsons-disease

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