I HAVE PARKINSON'S DISEASES AND THOUGHT IT WOULD BE NICE TO HAVE A PLACE WHERE THE CONTENTS OF UPDATED NEWS IS FOUND IN ONE PLACE. THAT IS WHY I BEGAN THIS BLOG.
I COPY NEWS ARTICLES PERTAINING TO RESEARCH, NEWS AND INFORMATION FOR PARKINSON'S DISEASE, DEMENTIA, THE BRAIN, DEPRESSION AND PARKINSON'S WITH DYSTONIA. I ALSO POST ABOUT FUNDRAISING FOR PARKINSON'S DISEASE AND EVENTS. I TRY TO BE UP-TO-DATE AS POSSIBLE.
I AM NOT RESPONSIBLE FOR IT'S CONTENTS. I AM JUST A COPIER OF INFORMATION SEARCHED ON THE COMPUTER. PLEASE UNDERSTAND THE COPIES ARE JUST THAT, COPIES AND AT TIMES, I AM UNABLE TO ENLARGE THE WORDING OR KEEP IT UNIFORMED AS I WISH.IT IS IMPORTANT TO UNDERSTAND I AM A PERSON WITH PARKINSON'S DISEASE. I HAVE NO MEDICAL EDUCATION,
I JUST WANT TO SHARE WITH YOU WHAT I READ ON THE INTERNET. IT IS UP TO YOU TO DECIDE WHETHER TO READ IT AND TALK IT OVER WITH YOUR DOCTOR. I AM JUST THE COPIER OF DOCUMENTS FROM THE COMPUTER. I DO NOT HAVE PROOF OF FACT OR FICTION OF THE ARTICLE. I ALSO TRY TO PLACE A LINK AT THE BOTTOM OF EACH ARTICLE TO SHOW WHERE I RECEIVED THE INFORMATION SO THAT YOU MAY WANT TO VISIT THEIR SITE.
THIS IS FOR YOU TO READ AND TO ALWAYS KEEP AN OPEN MIND.
PLEASE DISCUSS THIS WITH YOUR DOCTOR, SHOULD YOU HAVE ANY QUESTIONS, OR CONCERNS. NEVER DO ANYTHING WITHOUT TALKING TO YOUR DOCTOR FIRST..
I DO NOT MAKE ANY MONEY FROM THIS WEBSITE. I VOLUNTEER MY TIME TO HELP ALL OF US TO BE INFORMED.
I WILL NOT ACCEPT ANY ADVERTISEMENT OR HEALING POWERS, HEALING FROM HERBS AND ETC. UNLESS IT HAS GONE THROUGH TRIALS AND APPROVED BY FDA. IT WILL GO INTO SPAM.
THIS IS A FREE SITE FOR ALL WITH NO ADVERTISEMENTS
THANK YOU FOR VISITING! TOGETHER WE CAN MAKE A DIFFERENCE!
August 23, 2018, American Society for Biochemistry and Molecular Biology
A recent article in Molecular & Cellular Proteomics describes using new cell-surface markers to isolate a homogeneous mixture of dopamine precursor cells. The protocol may improve cell replacement therapy for Parkinson's disease. In this figure from the paper, the authors show that neurons induced from pluripotent cells that have been selected for expression of the newly described dopaminergic cell surface marker contactin 2 (top row) are more likely to express TH, an enzyme involved in dopamine production, and the dopamine transporter DAT, than unsorted cells (bottom row). Reducing the number of non-dopaminergic neurons and neural progenitors in a transplant improved recovery in a rat model and is expected to reduce side effects in patients with Parkinson's. Credit: Fathi et al. Parkinson's disease is a neurodegenerative disease that affects dopamine signaling neurons in patients' brains. Cell-replacement therapy shows some promise as a treatment for Parkinson's. A recent paper in the journal Molecular & Cellular Proteomics reports a technical advance in selecting cells to use in this therapy.Cell-replacement therapy involves differentiating stem cells into dopamine-signaling, or dopaminergic, neurons and transplanting them into a patient's brain to replace dying neurons. However, the variability of differentiated cells—including contamination with other neuronal cell types or residual undifferentiated stem cells—can affect transplantation outcomes. In clinical trials in the 1990s, for example, such contamination gave some patients severe dyskinesia, uncontrollable jerky movements that were worse than the movement problems caused by Parkinson's disease.To avoid interference by unwanted cell types, researchers need a differentiation protocol that yields a more homogeneous population of dopaminergic neurons. Researchers led by Hossein Baharvand, of Iran's University of Science and Culture in Tehran, and Ghasem Hosseini Salekdeh , of the Academic Center for Education, Culture and Research in Iran and Macquarie University in Australia, set out to develop such a protocol.First, the team developed a special stem cell line that contains a green fluorescent protein, or GFP, reporter for a transcription factor involved in dopaminergic neuronal development. In undifferentiated cells from this line, the fluorescent reporter is not expressed. When cells begin to make the transcription factor, the first step toward becoming a dopaminergic neuron, they also begin to make the GFP protein.The team then used standard protocols to differentiate the cells and sorted them by GFP expression. They then identified proteins that were enriched on the surface of partially differentiated cells called dopaminergic progenitors. By selecting for one protein characteristic of dopaminergic progenitors, called contactin 2, they isolated progenitors and transplanted them into rats modeling Parkinson's disease. Rats that received transplants with contactin 2-enriched cells had better dopamine release, indicating that the transplanted cells were a better match for the dying neurons they were meant to replace. Sorting the cells also reduced motor symptoms of Parkinson's compared with rats treated that received unsorted cells.The team's isolation procedure uses may be an important step toward more successful cell-replacement therapy.More information: Ali Fathi et al, Discovery of Novel Cell Surface Markers for Purification of Embryonic Dopamine progenitors for Transplantation in Parkinson's Disease Animal Models, Molecular & Cellular Proteomics (2018). DOI: 10.1074/mcp.RA118.000809Journal reference:Molecular & Cellular ProteomicsProvided by:American Society for Biochemistry and Molecular Biologyhttps://medicalxpress.com/news/2018-08-cell-therapy-parkinson-disease.html
August 23, 2018 by Charlene Betourney, University of Georgia
Lohitash Karumbaiah (center) and members of his laboratory. Credit: Justin Sharma
Researchers in the University of Georgia's Regenerative Bioscience Center have succeeded in reproducing the effects of traumatic brain injury and stimulating recovery in neuron cells grown in a petri dish. This makes them the first known scientific team in the country to do so using stem cell-derived neurons. The procedure, detailed in a new paper in Nature Scientific Reports, has significant implications for the study and treatment of such injuries.
Unlike other cells in the body, most neurons in the central nervous system cannot repair or renew themselves. Using an agent called glutamate that is released in high amounts in the brain after traumatic injury, the research team recorded a concussion-like disruption of neural activity in a dish containing dozens of minute electrodes. Through these recordings, they then evaluated the activity and influenced recovery by electrical stimulation.
"Once the neurons reach a certain level of density in the dish, you begin to see what we call synchronous activity in a very timed manner," said lead author Lohitash Karumbaiah, assistant professor in University of Georgia's College of Agricultural and Environmental Sciences Department of Animal Dairy Science. "Knowing we could re-create synchronized, brain-like activity in a dish gave us the impetus to ask, 'What if we disrupt this rhythm, and how can we recover from something like that?' "
In 2015, the U.S. Food and Drug Administration approved the first deep-brain stimulation device—an electrical stimulation cap that patients wear continuously—for treatment of Parkinson's disease. Karumbaiah and his team hope that electrical stimulation could be a clinically translatable approach for recovery from traumatic brain injury, or TBI. The next step, he said, is to connect with external collaborators to tailor electrical stimulation approaches with biomaterials that can exploit neuroplasticity.
Such treatments could be highly beneficial, for example, to veterans. Many veterans suffer from TBIs incurred through shock waves from explosions, with no physical focal point of injury. "Drilling into the brain randomly to access tissue in such cases makes no sense," said Karumbaiah. "A wearable device that can administer fairly controlled levels of relevant electrical stimulation can help these patients."
One of Karumbaiah's co-authors is Maysam Ghovanloo, professor of electrical and computer engineering at the Georgia Institute of Technology. Ghovanloo has led development of the Tongue Drive System, which allows individuals with spinal cord injuries to control their wheelchair or digital devices by moving their tongue. He has also developed technologies for neural interfacing and implantable medical devices. Ghovanloo will put his expertise in medical instrumentation to work in developing devices for the team's pre-clinical studies.
"We have developed a unique approach for observing and guiding stimulatory patterns in the brain at multiple levels, all the way from individual neurons to the neural tissue, and eventually the entire brain," Ghovanloo said. "All while taking into account the animal behavior to opportunistically apply stimulation when they are most effective."
According to Karumbaiah and Ghovanloo, electrical stimulation devices, whether designed for implantation or wearable use, must be small and power-efficient. They believe their approach will be clinically practical because smart design and application of stimulatory regimens can significantly reduce power consumption. "
"Because we've been recording from these neurons for a long time, we know what the magnitude of the pulses or activities of these neurons are," said Charles-Francois Latchoumane, a postdoctoral researcher in Karumbaiah's lab. "Now we can mimic those routines by programming them externally and feeding it back into the brain."
More information: Charles-Francois V. Latchoumane et al, Chronic Electrical Stimulation Promotes the Excitability and Plasticity of ESC-derived Neurons following Glutamate-induced Inhibition In vitro, Scientific Reports (2018). DOI: 10.1038/s41598-018-29069-3
August 23, 2018 by Kevin Jiang, Harvard Medical School
An MRI with increased signal in the posterior part of the internal capsule which can be tracked to the motor cortex consistent with the diagnosis of ALS. Credit: Frank Gaillard/Wikipedia
For decades researchers have worked to shed light on the causes of neurodegenerative disorders, a group of devastating conditions, including Alzheimer's and Parkinson's, that involve the progressive loss of neurons and nervous system function. In recent years, numerous factors, from genetic mutations to viral infections, have been found to contribute to the development of these diseases.
Yet age remains the primary risk factor for almost all neurodegenerative disorders. A precise understanding of the links between aging and neurodegeneration has remained elusive, but research from Harvard Medical School now provides new clues.
In a study published in Cell on Aug. 23, the research team describes the discovery of a molecular link between aging and a major genetic cause of both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), two related neurodegenerative diseases with shared genetic risk factors.
The findings, the researchers said, reveal possible new targets for treatment of these and other neurodegenerative diseases.
"Our study provides the first description of a molecular event that connects aging with neurodegeneration," said senior study author Junying Yuan, the HMS Elizabeth D. Hay Professor of Cell Biology. "These insights are a critical step towards understanding the mechanisms by which aging predisposes individuals to neurodegeneration."
The results also highlight the need for a better understanding of the biology of neurodegenerative diseases in the context of aging.
"Laboratory models of neurodegenerative diseases often have a missing element, and that is the contribution of age," Yuan said. "We have to understand better the process in its totality, not just its isolated components, to better guide clinical trials and improve our chances of finding effective treatments for these devastating diseases."
RIP rescue
Also known as Lou Gehrig's disease, ALS is a progressive, incurable condition marked by the gradual death of motor neurons. It shares some clinical and genetic features with FTD, which is marked by an early and rapid onset of dementia.
Around one in 10 patients with both diseases carry genetic mutations that cause the partial dysfunction of a protein known as TBK1. Previous studies, including by Yuan and colleagues, have shown that TBK1 is involved in a form of programmed cell death and in neuroinflammation, a hallmark of neurodegenerative disorders.
How TBK1 contributes to the development of ALS and FTD, however, was unclear.
In the current study, Yuan and colleagues modeled the reduced levels of TBK1 found in ALS and FTD patients by creating mice that had only one functional copy of the gene that produces TBK1. These mice were healthy and similar in appearance to normal mice. In contrast, those that lacked the gene entirely died before birth.
However, the team found that mice without TBK1 could be fully rescued—surviving birth and becoming healthy adults—by blocking the activity of RIPK1, another protein known to play a central role in programmed cell death, neuroinflammation and neurodegenerative disease. Further analyses revealed that TBK1 normally functions to inhibit the activity of RIPK1 during embryonic development.
This discovery prompted the researchers to investigate another protein, called TAK1, previously known to also inhibit RIPK1 function. When they looked at data on TAK1 expression in human brains, the scientists found that TAK1 expression declines significantly with age. In the brains of patients with ALS, TAK1 expression was further reduced compared with the brains of similarly aged people without ALS.
Brake it down
To model the interaction between partial loss of TBK1 and TAK1 with aging, the team created mice that expressed half the usual amount of TBK1. The mice also expressed half the usual amount of TAK1 in their microglia, the immune cells of the brain where TAK1 is normally most active.
With reductions in both TBK1 and TAK1, these mice displayed traits associated with ALS and FTD, including motor deficits, hind limb weakness, anxiety-like behavior in new environments and changes in brain chemistry. The mice had a reduction in the number of neurons in the brain, and increased motor neuron dysfunction and cell death.
When the team inhibited RIPK1 activity independently of TBK1 and TAK1, they observed a reversal in symptoms.
Like a pair of brakes on a bicycle, TAK1 and TBK1 appear to work together to suppress the activity of RIPK1, and even if one brake fails, the other can compensate, the researchers said. But if both begin to fail, RIPK1 activity increases, leading to cell death and neuroinflammation.
This may be why individuals with TBK1 mutations do not develop ALS and FTD until they become older, when TAK1 levels decline with age, Yuan said.
Several clinical trials are underway to test the safety and efficacy of drugs that block RIPK1 activity in neurodegenerative and chronic inflammatory diseases, and these findings support the rationale for those trials, Yuan added.
"I think the next couple of years will reveal whether RIPK1 inhibitors can help ALS and FTD patients," she said. "I think our study makes us more confident those efforts might work."
Despite numerous large-scale clinical trials, however, no effective therapeutics have yet been developed for neurodegenerative diseases. This research now establishes a model of study that incorporates both aging and genetic risk for ALS and FTD, which may have broad implications.
"Many trials have been launched based on data from studies in mice, but how can a two-year-old mouse, for example, fully reflect what happens in an 80-year-old patient with Alzheimer's?" Yuan said. "We need to develop new thinking on how to model these diseases to incorporate the element of aging, and we think this study is an important step toward that goal."
The scientists are currently investigating why TAK1 levels decline with age and its potential role in other neurodegenerative diseases.
More information: Daichao Xu et al, TBK1 Suppresses RIPK1-Driven Apoptosis and Inflammation during Development and in Aging, Cell (2018). DOI: 10.1016/j.cell.2018.07.041
Immunohistochemistry for alpha-synuclein showing positive staining (brown) of an intraneural Lewy-body in the Substantia nigra in Parkinson's disease. Credit: Wikipedia
Tremor, rigidity and bradykinesia are well known symptoms of Parkinson's disease, occurring in different combinations in individual patients. However, there have not been any neuronal components that definitively identify the main symptom groupings – including tremor-dominant forms and those without tremor – that can be used to guide treatment approaches.
In a new study, researchers at Baylor College of Medicine have now found neural correlates of two main Parkinson's disease phenotypes that could lead to more precise or personalized deep brain stimulation treatments or future neuromodulation technologies to treat this disorder.
The findings appear in the latest edition of the Proceedings of the National Academy of Sciences.
The study focuses on the subthalamic nucleus, a part of the brain that makes up the basal ganglia system, which contributes to motor control, learning and carrying out behaviors and emotions. It is an area that is associated with certain movement disorders, and is one of the areas that is frequently targeted in the use of deep brain stimulation to treat Parkinson's disease.
"It is an area believed to show electrophysiological abnormalities that accompany the motor symptoms, but very limited data exists," said Dr. Joohi Jimenez-Shahed, associate professor of neurology and director of the Deep Brain Stimulation Program at Baylor. "In our study, we were able to find distinct patterns between these two most common phenotypes when recording local field potentials of the subthalamic nucleus."
Local field potentials are signals made by the combined activity of a group of neurons. Researchers studied 24 patients with Parkinson's disease, dividing them into two groups based on the physical symptoms – tremor-dominant or postural instability and gait difficulty subtypes. By analyzing recordings from multiple microelectrodes in sub-territories of the subthalamic nucleus, they were able to record electrophysiological abnormalities that distinguished between the two sets of motor symptoms.
"Deep brain stimulation of this region is an effective therapy for the treatment of these motor symptoms, but an important goal during this type of surgery is placement of the electrode within the motor territory of the subthalamic nucleus in a location that leads to the greatest therapeutic effect," Jimenez-Shahed said. "Our findings demonstrate the feasibility of using microelectrode local field potentials to identify physiological signatures of Parkinson's disease symptoms to further pinpoint these areas."
Researchers also added that being able to identify these precise areas could lead to more individualized treatment for each patient, thereby resulting in greater benefits and fewer side effects.
More information: Ilknur Telkes et al. Local field potentials of subthalamic nucleus contain electrophysiological footprints of motor subtypes of Parkinson's disease, Proceedings of the National Academy of Sciences (2018). DOI: 10.1073/pnas.1810589115
A whey protein-based nutritional supplement improved motor functions in patients with Parkinson’s or parkinsonism who were engaged in an intensive physical rehabilitation program, according to clinical trial results.
Physical rehabilitation is a relevant approach for the treatment of motor impairment in patients with Parkinson’s or parkinsonism, a general term for neurological disorders that cause movement problems similar to those of Parkinson’s disease patients.
In the elderly, scientists have shown that muscle-targeted nutritional support can increase muscle mass and improve physical performance. However, no such evidence is available in patients with parkinsonian syndromes, which include Parkinson’s, progressive supranuclear palsy and multiple system atrophy, among other conditions, and are characterized by muscle dysfunction, especially weakness.
Researchers conducted a randomized clinical trial (NCT03124277) in Milan, Italy, testing the effectiveness of a specific regimen of muscle-targeted nutritional support on the functional status of patients with Parkinson’s or parkinsonism undergoing a multidisciplinary intensive rehabilitation treatment (MIRT).
The trial included 150 patients (children, adults and elderly) who received a standard hospital diet with or without a nutritional supplement called FortiFit (developed by Nutricia). Per serving (40 grams), the supplement includes 20 grams whey protein (found in dairy products), 800 IU vitamin D, 3 g total leucine (an essential amino acid, meaning it cannot be naturally produced by the body), 9 g carbohydrates, 3 g fat, and a mixture of vitamins, minerals and fibers.
Patients took the supplement twice daily for 30 days.
The team primarily focused on changes in the 6-minute walking test (6MWT), an assessment of exercise capacity. They also analyzed gait speed (with the 4-minute walking test), handgrip strength, Berg balance scale, the Self-assessment Parkinson’s Disease Disability Scale — exploring self-perceived functional status — and the timed up-and-go test (TUG), which is a measure of mobility and balance. The TUG test evaluates the time taken to stand up from an arm chair, walk a distance of three meters, turn, walk back, and sit down.
Body weight and skeletal muscle mass (SMM) also were determined.
Patients who received the supplement experienced a greater increase in the distance walked in the 6MWT (mean 69.6 vs. 51.8 meters without the supplement). When accounting for changes in dopaminergic therapy as well as in SMM, the team found a similar 18.0 meters difference.
Taking the supplement also improved gait speed (0.07 m/s), TUG test score (-1.1 s), and SMM (0.5 kg).
“In patients with [Parkinson’s] or parkinsonism, the consumption of a whey protein-based nutritional formula enriched with essential amino acids and vitamin D improved the efficacy of a MIRT, particularly lower body physical function,” researchers concluded.
Apathy is prevalent problem in Parkinson’s disease, but it is more evident in patients’ behavioral and social habits than in their emotional or cognitive ones, researchers in the U.K. report.
Apathy is a well-recognized Parkinson’s non-motor symptom, although research rarely looks into the specific domains – behavioral, cognitive, executive, social, and emotional – it affects, or how exactly this symptom relates to depression and anhedonia (the inability to feel pleasure) seen in Parkinson’s patients.
University of Oxford researchers used the Apathy Motivation Index (AMI), a self-report measure of apathy validated in healthy individuals, to examine the multidimensional profile of apathy in Parkinson’s disease.
AMI categorizes apathy according to behavioral (the tendency to self-initiate goal-directed behavior), social (the level of engagement in social interactions), and emotional (ability to express feelings or affective responses) domains.
The team first evaluated AMI’s reliability and validity in Parkinson’s by comparing it with the Lille Apathy Rating Scale (LARS), a well-validated interview approach to assessing apathy in Parkinson’s and used in the development of AMI. Next, they evaluated if Parkinson’s patients exhibited differences in apathy domains compared to healthy controls, and if these domains associated with depression and anhedonia.
The study included 102 Parkinson’s patients (mean age 67.7; 79 men) and 147 healthy volunteers (mean age 66.1; 104 men). Mean disease duration was 6.6 years and Unified Parkinson’s Disease rating scale score was 27.0 (on a 0-199 scale, with 0 meaning no disability and 199 total disability). Neither patients nor controls had other neurological or psychiatric conditions.
Eighty-seven patients completed LARS, 84 (and 67 controls) completed the 14-item Snaith–Hamilton Pleasure Scale (SHAPS, a 14 item scale that measures anhedonia), and 80 (87 controls) completed the Geriatric Depression Scale–Short Form (GDS-15, a 15-item form to screen for depression in a variety of settings).
Results showed that AMI’s total score correlated positively with LARS’ overall score, demonstrating good construct validity, the researchers said. AMI also showed diagnostic accuracy in identifying 36 Parkinson’s patients with apathy. According to the authors, this means that AMI enables them to explore the various dimensions of apathy, while achieving an apathy prevalence rate consistent with existing studies.
Parkinson’s patients showed a higher total AMI score than healthy controls, indicating greater apathy overall. This result, as well as individual subscale scores, was not dependent on age, sex, cognition, years of education, disease duration, and levodopa doses.
Subsequent analyses revealed that patients had higher levels of behavioral and social apathy relative to controls, but not of emotional apathy. However, six patients showed deficits in emotional sensitivity and no deficits in the other domains.
Patients who were more behaviorally and socially apathetic were more likely to be depressed, a co-existing condition not observed in emotional apathy scales among patients. In healthy controls, higher the level of emotional apathy associated with lower the evidence of depression.
“This result suggests that different clinical approaches toward apathy in patients with PD compared to the general population might be needed,” the scientists wrote.
Patients with higher behavioral and social apathy also showed more evidence of anhedonia. Again, this was not found in emotional apathy. In the controls, only social apathy correlated with a reduced capacity to feel pleasure. No differences were found between patients and controls regarding anhedonia levels.
“Together our findings may help in guiding the development of more effective, selective treatments for apathy in [Parkinson’s] — including nonpharmacological ones aimed at different aspects of motivation — as well as assisting in our understanding of how apathy, anhedonia, and depression are related,” the researchers concluded.
Tremor, rigidity and bradykinesia are well known symptoms of Parkinson’s disease, occurring in different combinations in individual patients. However, there have not been any neuronal components that definitively identify the main symptom groupings – including tremor-dominant forms and those without tremor – that can be used to guide treatment approaches.
In a new study, researchers at Baylor College of Medicine have now found neural correlates of two main Parkinson’s disease phenotypes that could lead to more precise or personalized deep brain stimulation treatments or future neuromodulation technologies to treat this disorder.
The study focuses on the subthalamic nucleus, a part of the brain that makes up the basal ganglia system, which contributes to motor control, learning and carrying out behaviors and emotions. It is an area that is associated with certain movement disorders, and is one of the areas that is frequently targeted in the use of deep brain stimulation to treat Parkinson’s disease.
“It is an area believed to show electrophysiological abnormalities that accompany the motor symptoms, but very limited data exists,” said Dr. Joohi Jimenez-Shahed, associate professor of neurology and director of the Deep Brain Stimulation Program at Baylor. “In our study, we were able to find distinct patterns between these two most common phenotypes when recording local field potentials of the subthalamic nucleus.”
Local field potentials are signals made by the combined activity of a group of neurons. Researchers studied 24 patients with Parkinson’s disease, dividing them into two groups based on the physical symptoms – tremor-dominant or postural instability and gait difficulty subtypes. By analyzing recordings from multiple microelectrodes in sub-territories of the subthalamic nucleus, they were able to record electrophysiological abnormalities that distinguished between the two sets of motor symptoms.
“Deep brain stimulation of this region is an effective therapy for the treatment of these motor symptoms, but an important goal during this type of surgery is placement of the electrode within the motor territory of the subthalamic nucleus in a location that leads to the greatest therapeutic effect,” Jimenez-Shahed said. “Our findings demonstrate the feasibility of using microelectrode local field potentials to identify physiological signatures of Parkinson’s disease symptoms to further pinpoint these areas.”
Researchers also added that being able to identify these precise areas could lead to more individualized treatment for each patient, thereby resulting in greater benefits and fewer side effects.
Others who contributed to the study include Ilknur Telkes, first author, the University of Houston; Ashwin Viswanathan, Department of Neurosurgery at Baylor; Joseph Jankovic, director of the Parkinson’s Disease Center and Movement Disorders Clinic at Baylor; Aviva Abosch, the University of Colorado School of Medicine; Musa Ozturk, the University of Houston; Akshay Gupta, the University of Minnesota Medical School; and Nuri F. Ince, lead author, the University of Houston. The research was conducted using a novel intraoperative neural data acquisition and signal processing system developed by Ince.
For Funding Information: http://www.pnas.org/content/early/2018/08/20/1810589115
A charity walk around Norfolk’s coastline has raised more than £60,000 to help find a cure for Parkinson’s disease.
Tim Daber leads the way along the Norfolk Coast Path. Picture: Chris Bishop
Tim Daber and friends set off from Sea Palling on Saturday morning. They arrived at Hunstanton four days later, this afternoon.
“I’m tired but pleased,” said Mr Daber, as he crossed the finishing line at the Hunstanton Lawn Tennis Tournament off the Cromer Road.
“I’m wondering what I’m going to do after this.”
Mr Daber’s walk for the Cure Parkinson’s Trust took months of planning. He chose to walk 60 miles of Norfolk’s coastline to mark his 60th birthday.
The walkers take a breather near Holme. Picture: Chris Bishop
Mr Daber was diagnosed with Parkinson’s two years ago. The neurological condition, which slows movement and makes everyday activities increasingly difficult, is currently incurable.
Up to one in 37 people are expected to be diagnosed with it in later life.
“I heard in April last year that a cure could be found with the right investment, in the lifetime of some of the people who have the disease,” said Mr Daber. “It was a jaw-dropping moment. I decided I had to do something.”
Statins are a class of drugs prescribed to prevent heart attacks and strokes. The drug works by blocking the liver enzyme responsible for the production of cholesterol. By doing this, the drug lowers your body’s cholesterol levels and decreases your risk for cardiovascular conditions.
Some medical professionals have come to attribute statins with neuroprotective effects, but the authors of the study say the evidence for this is inconclusive at best.
She adds that the research on the neuroprotective properties of statins has so far involved just cell cultures and animal models.
For their research, Huang and her colleagues looked at medical insurance claim data from 50 million people. They identified how long it took before the first symptoms of Parkinson’s appeared since the patients began taking statins. They found that there was indeed a correlation between the use of statins and a higher risk of developing Parkinson’s.
Mother Nature's micronutrient secret:
Organic Broccoli Sprout Capsules now available, delivering 280mg of high-density nutrition, including the extraordinary "sulforaphane" and "glucosinolate" nutrients found only in cruciferous healing foods. Every lot laboratory tested.
Furthermore, they saw that most patients manifested symptoms within 2.5 years of treatment with statins. Most of these cases involved the use of lipophilic or fat-soluble statins, one of the two versions of the drug available in the market today.
As its name suggests, lipophilic statins diffuse in fat or lipids, unlike their hydrophilic counterparts that diffuse in water.
The former is noted for its ability to distribute across a wider range of tissues. It can even reach the brain while the latter cannot. This has made lipophilic statins more popular, as evidenced by the greater number of names they are marketed as, such as atorvastatin, fluvastatin, lovastatin, cerivastatin, pitavastatin, and simvastatin.
Huang explained that contrary to prior belief that halting statins causes the development of Parkinson’s disease, it is the drugs themselves that cause the symptoms to manifest in the first place. She admits that further research is needed to fully understand the results of their research, but that their findings prove that patients need to be careful before taking statins.
“Statin use was associated with higher, not lower, Parkinson’s disease risk, and the association was more noticeable for lipophilic statins, an observation inconsistent with the current hypothesis that these statins protect nerve cells,” she says.
As mentioned previously, lipophilic statins make it to the brain. When they do, they cross the blood-brain barrier, the mechanism that filters the substances that enter the brain and give patients insomnia. Other patients have complained of memory loss and confusion. The effects are more pronounced among patients with dementia.
Statins have also been linked to muscle pain and damage, leading patients to feel sore, tired, or weak in the affected areas. This particular side effect is actually one of the major reasons many patients opt out of statins.
Lohitash Karumbaiah (center) and members of his laboratory. Credit: Justin Sharma
The walkers take a breather near Holme. Picture: Chris Bishop
The walkers take a breather near Holme. Picture: Chris Bishop
