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!
A research team at the Kyoto University’s Center for iPS Cell Research and Application is delaying a possible therapy for Parkinson’s disease, saying it will likely not apply for safety screening before next year.
If approved, the therapy would be the world’s first application of iPS cells for sufferers of the degenerative disease.
A research team at the center initially planned to apply for screening by a third-party panel at the university as early as this June. It pushed back the plan when it revised its clinical research plan, the center said.
The team, led by professor Jun Takahashi, initially planned to create iPS cells, or induced pluripotent stem cells, from a patient’s blood cells and grow them into neurons for transplanting into the patient’s brain. The results would be closely monitored, including whether the procedure induces a brain tumor.
Parkinson’s disease reduces neurons in the brain and results in tremors in hands and feet and stiffness of the body.
When a new source of iPS cells became available in August, the center decided to push back its clinical research to make use of the newly available cells.
Last year, a separate Japanese research team successfully transplanted retinal cells grown from iPS cells into a woman.
invented a spill proof cup for her grandfather whose unsteady hands were causing him to spill drinks.
Lily Born of Chicago began imaging solutions a few years ago dreaming of ways to help him cope better with Parkinson’s. Then, she had an idea to attach legs onto his tumbler to prevent it from spilling. The Kangaroo Cup was born.The first ceramic version proved too breakable and uncomfortable to hold so Lilly and her parents went back to the drawing board. This week they have successfully raised money with an online Kickstarter campaign to fund the improvements.
The new cups made with moldable prototyping plastic are stackable, unbreakable, and microwave & dishwasher safe. Still tip-resistant, the new three-legged design has an elevated base reducing the need for a coaster, and is made with BPA-free plastic.
The campaign is essentially pre-selling the 9-ounce cups — for instance, a set of four for $25. They already have raised $37,000 with still 26 days to go.
“Just because you’re a kid, doesn’t mean you can’t do big and great things’, the pre-teen designer says
Parkinson’s disease may soon be able to treat their own tremors and muscle stiffness without invasive therapy or even a trip to the doctor’s office.
A headband-shaped device can deliver daily, noninvasive brain stimulation at home and tamp down Parkinson’s symptoms.
While the prototype, developed by biomedical engineering graduate students at Johns Hopkins University, hasn’t yet been tested on humans, it’s seen as a promising first step toward helping Parkinson’s patients safely relieve their own symptoms.
David Blumenstyk, one of the student inventors, demonstrates how the noninvasive brain stimulation prototype fits. (Credit: Will Kirk/Johns Hopkins)
Parkinson’s is an incurable neurodegenerative disorder that affects 1 million people in the United States and 7 million worldwide.
PAINLESS TREATMENT
For patients in advanced stages of the disease, one treatment option is deep brain stimulation, in which a surgeon implants thin electrical leads into the brain. A pulse generator—similar to a heart pacemaker—goes under the skin and sends electrical signals to the brain.
“We saw that this procedure is really invasive and can take 10 to 15 hours to complete,” says Shruthi Rajan, a team member. “It’s also very expensive, and not all patients qualify for the surgery. We asked if there was a way to provide the same treatment in a less invasive way that doesn’t require brain surgery.”
The students were referred to Yousef Salimpour, a Johns Hopkins Medicine postdoctoral research associate studying a noninvasive Parkinson’s therapy called transcranial direct current stimulation.
In this painless treatment, low-level current is passed through two electrodes placed over the head to tweak electrical activity in specific areas of the brain. The technique can be used to excite or inhibit these nerve cells. The treatment is experimental, but has attracted attention because it does not require surgery and is inexpensive, safe, and relatively easy to administer without any side effects.
TOUCH OF A BUTTON
The biomedical engineering students met with Salimpour. “We told him we had an idea for a portable home version of this equipment,” Rajan says. “But we planned to add safety measures to make sure the patient used it properly without a doctor or nurse being present.”
The students aimed for a prototype that would enable a patient to activate the battery-powered treatment by touching a large, easy-to-press button. The students designed their prototype to deliver current for only 20 minutes daily and only at a doctor-prescribed level.
Dozens of Parkinson’s patients helped the students craft the headband so it would be easy to put on, comfortable, and positioned correctly on the head.
“For a comfortable fit, we put an elastic band in the back and told the patients to put it on like a baseball cap,” team member Ian Graham says. “The interaction with the patients was really helpful.”
REMOTE ADJUSTMENTS
The students also received guidance from other members of an interdisciplinary team of Johns Hopkins medical researchers.
“Our group is working on the idea of using noninvasive brain stimulation for Parkinson’s disease symptom control as a new clinical treatment,” Salimpour says. “Our preliminary results were promising. Patients keep asking us for more of this treatment.
“But we couldn’t provide the treatment for them because there is no portable and FDA-approved device like this for Parkinson’s patients that is on the market at this time. The biomedical engineering students then approached us with the idea of designing the home-based treatment device. They did a great job, and made a fascinating prototype. We hope that based on their preliminary work, Parkinson’s patients will receive the benefit of this new technique at home very soon.”
Lund University researchers have shown that cerebrospinal fluid (CSF) biomarkers of angiogenesis are raised in Parkinson’s disease (PD) patients and are related to walking and balance difficulties, blood-brain barrier (BBB) increased permeability, and white matter lesions (WMLs). The research study, entitled “Increased CSF biomarkers of angiogenesis in Parkinson Disease” was published in Neurology.
Angiogenesis, i.e., the formation of blood vessels, has been linked to PD pathogenesis — post mortem analysis of patient’s brains has identified increased numbers of nuclei from endothelial cells, blood vessels and increased levels of specific angiogenesis biomarkers. But angiogenesis’ role in PD is not yet completely established and understood. As such, the scientists used biological assays to measure different biomarkers of angiogenesis in CSF samples from PD patients with and without dementia, and compared them to disease-free controls. Additionally, the correlation of these markers’ levels with balance problems (a frequent PD symptom), BBB permeability, and brain lesions was also investigated.
In the first part of the study, 100 PD patients and 38 healthy controls were assessed, with results further repeated in two similar-size groups of patients. The analysis showed that in PD patients with or without dementia, VEGF (vascular endothelial growth factor), PlGF (placental growth factor), and sVEGFR-2 (a VEGF receptor) levels were elevated while Ang2 (angiopoietin 2) levels were decreased when compared to healthy controls.
The data is in line with previous findings of angiogenesis evidence in PD, and with the fact that Ang2 factor is associated with BBB stability maintenance. Moreover, VEGF has been shown to induce vascular leakage and increased BBB permeability (BBB dysfunction is associated with the onset of PD). In BBB dysfunction, blood components can leak into the brain and cause tissue lesions, leading to neuronal damage and neurodegeneration.
Researchers found that PD patients with orthostatic diastolic hypotension, which might lead to episodes of cerebral hypoxia (low oxygen levels), also present increased levels of VEGF and PlGF when compared to PD patients without this pathology. Hypoxia has been hypothesized as one of the main causes of angiogenesis in the brain, a theory that can be corroborated with this study’s findings of elevated angiogenic factors. The same correlation was found for white matter lesions (WMLs), which are associated with posture instability and walking problems, significantly more pronounced in PD patients’ brain with elevated angiogenesis biomarkers. Moreover, increased levels of VEGF and PIGF were correlated with increased markers of neurodegeneration.
In the future, researchers intend to test angiogenesis drugs in animal models as possible therapies for Parkinson’s disease treatment. “Medication for angiogenesis already exists. If we can confirm our results in further studies, these drugs can be tested on Parkinson’s patients in the future,” Dr. Oskar Hansson, reader at the Lund University, Sweden, said in a press release.
In a new study examining patients with advanced Parkinson’s disease, neurologists say they’ve identified parts of the brain that control placebo effect, raising hopes of singling out people most susceptible.
But they’re still very much in the dark about underlying causes of one of medicine’s great mysteries. Some people, when given fake treatment, actually get better, but others, for whatever reason, do not. Stranger still, some people improve at the mere suggestion of future treatment.
The placebo effect is a problem for clinical researchers because they need to know which treatments work and which don’t. When people respond well to treatments they aren’t actually given or that don’t actually work, it skews the results. That’s why, for years, doctors have been trying to figure out how placebo works and why.
“While they may appear to be mysterious, placebo responses have discernible neurophysiological mechanisms,” wrote the authors of a companion commentary in The Journal of Clinical Investigation. To learn more about those mechanisms, neuroscientists at the Feinstein Institute for Medical Research in New York chose 45 patients with Parkinson’s disease for a double-blind study. All of them would receive brain surgery, but only 22 would receive actual treatment. The other 23 were given fairly routine operations designed to do nothing.
The doctors weren’t looking for signs of placebo effect — they already knew it would happen. Patients with Parkinson’s disease, the second most common neurological illness behind Alzheimer’s, have previously shown an incredible sensitivity to the idea of treatment. A 2001 study illustrated that dopamine released at the expectation of possible healing had healing benefits by itself. “Expectations,” doctors wrote in another study, “have a strong influence on the subsequent emotional experience of both” pain relief and reward processing.
Instead, what David Eidelberg and colleagues at the Feinstein Institute were looking for was what happened inside their brains before and after the brain surgery. Using PET scans, they measured activity in parts of the brain associated with negative emotions, expectancy and placebo-induced anti-depressive effects. After the placebo surgery, 16 of the 23 patients performed better on tests of their motor functioning. Seven saw no improvement.
Here’s the interesting thing: Those 16 patients had very little activity before surgery in the parts of the brain that are activated by placebo. The other seven had more activity in the region all along. So that’s the good thing — research doctors may now have something to look for when they want to weed out placebo-receptive test patients.
The bad thing is researchers still have no clue how a little dopamine and anti-depressant brain activity relates to improved motor function. “The final effector pathway remains obscure,” wrote Mariya V. Cherkasova and A. Jon Stoessl in their commentary. But they say one thing is more clear from the study — expectation didn’t have anything to do with it. The knowledge of participation in clinical trials did not induce placebo effect.
In a sad coda to the study, one year after their placebo brain surgeries, the Parkinson’s patients were unblinded. That is, their doctors revealed that they had been in the sham surgery group and not the treatment group. Immediately, the parts of their brains that are activated by placebo reverted to their normal state. With that, their small gains in motor functioning disappeared, too.
The Italian artist, engineer and scientist Leonardo da Vinci (1452-1519) also studied anatomy, physiology and medicine. Leonardo da Vinci kept secret notebooks in which he wrote and sketched his ideas and observations, in handwriting that only he could read. So keen was he to study the human body that he went out at night to dissect human corpses. For more information go to Leonardo da Vinci.
Over 300 years before James Parkinson formally described Parkinson's Disease, Leonardo da Vinci saw people whose symptoms coincided with those seen in Parkinson's Disease. Leonardo wrote in his notebooks that "you will see.....those who.....move their trembling parts, such as their heads or hands without permission of the soul; (the) soul with all its forces cannot prevent these parts from trembling." In a translation of Da Vinci's notebooks "The movements of paralytics of those benumbed by cold, whose head and members move without control of the soul, who cannot stop the movements." The combination of difficulty with voluntary movement ("paraletici") and tremor ("tremanti') leave little doubt of the diagnosis of Parkinson's Disease.
At the end of his life Leonardo was unable to paint due to the loss of control of movement in his hands. It has been suggested that, by then, Leonardo da Vinci had Parkinson's Disease himself. Due to most of his notebooks remaining secret for centuries, Leonardo did not receive any credit for contributing to the recognition of Parkinson's Disease.
Researchers' quest to understand a worm's strange behavior yields important information on dopamine receptor signaling.
Several years ago, University at Buffalo biologists noticed something odd.
They were studying how a worm called C. elegans would react when different genes were deleted from its DNA. One particularly interesting deletion resulted in nematodes with a heightened sense of smell: They backed away from repulsive odors unusually fast.
The lead researchers, Denise Ferkey and Michael Yu, took note; they had seen this behavior before.
In prior, unrelated experiments, the same species of worm had become hypersensitive to smell when its nerve cells experienced problems with dopamine signaling, a cellular process that helps control how readily cells can communicate with one another.
The researchers wondered: Was a similar issue at play again?
That question -- and that curiosity -- led the scientists on a multi-year research project that could one day open new treatment avenues for diseases ranging from schizophrenia to Parkinson's.
Missing gene alters dopamine signaling
On Nov. 10 in the journal Science Signaling, Ferkey and Yu's team reported that the mutant worms they were studying had altered dopamine signaling because the animals were missing the gene for an enzyme called PRMT-5, which facilitates another important cellular process -- protein arginine methylation.
When researchers took the gene away, the worms stopped making PRMT-5; protein arginine methylation decreased; and dopamine signaling declined as a result. The scientists also discovered that the same mechanism -- arginine methylation -- regulates dopamine signaling in human cells.
"We're excited about this finding because dopamine signaling is involved in such a diversity of biological processes," says Ferkey, PhD, an associate professor of biological sciences in the UB College of Arts and Sciences. "We also know that it's linked to Parkinson's disease, schizophrenia and drug addiction. Our research opens up possibilities for a whole new class of drugs."
"One of the interesting things we saw in our study was that dopamine signaling became weaker, but it didn't turn it off completely," says Yu, PhD, UB associate professor of biological sciences. "A lot of treatments take an all-or-nothing approach: You either have something or you don't. But with arginine methylation, we may be able to take a softer approach and fine-tune how powerful the signaling is."
"From the standpoint of pharmaceuticals, modulation is good because it could reduce side effects," Ferkey adds. "The body may respond better to fine-tuning than to a sledgehammer."
A versatile avenue for therapeutics
Dopamine is a neurotransmitter -- a chemical that plays an important role in how nerve cells respond to stimuli and communicate with one another.
Produced naturally in the brain, dopamine has become a neuroscience rock star: It's involved in how the mind registers rewards, and media have reported on the chemical's connection to addiction, gambling and pleasure. Dopamine is also involved in many other biological processes, including an array of diseases.
One way dopamine influences intercellular communication is by binding to receptors found in nerve cells, an action that can influence how likely these cells are to 'fire' and communicate messages to other cells.
Ferkey and Yu's team traced how the PRMT-5 enzyme affects this process. In doing so, they show how versatile their discovery could be in pursuing treatments for diverse diseases.
PRMT stands for 'protein arginine methyltransferase,' and PRMT enzymes facilitate the chemical process of arginine methylation, the fastening of a methyl group (made from one carbon and three hydrogen atoms) to proteins inside cells.
Arginine methylation is crucial to many bodily functions, but until now, scientists did not know it mattered in dopamine signaling, said Yu, whose research focuses on PRMTs.
His and Ferkey's new study found that PRMT-5 helps a methyl molecule attach to dopamine receptors called D2-like receptors in nerve cells. With the methyl group attached, the receptors emit stronger signals, responding more powerfully when dopamine molecules latch on.
This influences the sensitivity of the nerve cells, changing how likely they are to communicate important messages to other cells.
This held true in both worm cells and human cells, which shows that the role of PRMTs in dopamine signaling has been conserved through evolution -- a quality that often points to a particularly useful adaptation.
The dopamine receptors the researchers studied belong to a family called G protein-coupled receptors (GPCRs), and the newly discovered PRMT-5 mechanism may be active on hundreds of these receptors -- creating huge potential for new therapeutics.
A win for basic science
A side effect of losing PRMT-5 in C. elegans is a heightened sense of smell: In the worms, dopamine signaling acts as a brake or check on the sensory system's response to odorants. So when you remove PRMT-5 and diminish dopamine signaling, the brake comes off and the mutant worms react more strongly to odor, Ferkey says.
"Our study is a big win for basic science research," she says. "We didn't set out to identify a new means of regulating dopamine signaling. We saw this very curious phenotype -- this mutant worm with this heightened sense of smell -- and remembered it from previous experiments dealing with something totally different."
"Many of science's great findings are serendipitous," Yu adds. "Our story shows why it's so important for society to support basic science research."
Parkinson's Disease (PD) patients have a five-fold greater risk of carrying genetic mutations in the β-glucocerebrosidase gene (GBA), which are commonly associated with Gaucher disease (GD). Patients with both PD and GD tend to experience earlier onset of PD and more serious cognitive changes than PD patients without the mutations. A new study published in the Journal of Parkinson's Disease suggests that GD or the presence of GBA mutations may actually shield patients from deficiency in visual color discrimination, which is a hallmark of PD.
"Consistent with previous studies, color discrimination was decreased in patients with PD. However, this study introduces new findings that relate to the impact of GD in the context of PD-related color discrimination. These findings may imply a 'protective effect' on color discrimination in those GD patients who also have PD, which probably is due to a sensory mechanism rather than a cognitive effect," explained lead investigator Deborah Elstein, PhD, of the Gaucher Clinic at Shaare Zedek Medical Center Jerusalem (Israel), which is the largest clinic of its kind, devoted solely to Gaucher disease patients. This group, spearheaded by Prof. Ari Zimran, the Director of the Gaucher Clinic, was the first to publish anecdotal evidence of the association between GD and early-onset PD.
The investigators tested groups of patients on a color visual discrimination test known as the Farnsworth-Munsell 100 hue test (FMHT) and calculated their mean Total Error Scores (TES). In the FMHT, patients are asked to arrange colored caps so that there is a gradual transition in color between two anchor caps of different colors. Better performance is indicated by lower TES scores.
The groups consisted of 10 patients each, classified by PD only, GD only, both PD and GD, carriers of the GBA mutations, GBA carriers with PD or healthy controls. GBA carriers were thought to have one mutation whereas those with GD have two mutations.
Looking at the mean number of errors on the FMHT, the GD only group made the least number of errors (mean 129.70), fewer errors than even the healthy controls (mean 177.70). The PD only group made the most number of errors (mean 289.70), more than twice the number made by those with GD only, confirming that PD patients manifest poor color discrimination.
Patients with both GD and PD made the second highest number of errors (mean 237.90), followed by those who were GBA carriers with PD (220.20). GBA carriers without PD made more errors (177.20) than those with GD only, which was approximately the same number of errors as healthy controls. Overall, patients with PD displayed worse visual color discrimination compared to those without PD.
"The seminal finding of lowest TES (fewest errors) among patients with GD only (also relative to the healthy persons) was unexpected," stated Dr. Elstein. She also noted with interest that patients with GD (with or without PD) had lower TES than GBA carriers (with or without PD).
These findings strengthen the evidence linking PD and GD. For instance, a small proportion of patients with GD, and an even higher proportion of their relatives who are carriers of GD, display symptoms of parkinsonism. Other studies have found that having one or two mutations of the GBA gene is a risk factor for PD, while PD patients have a greater than anticipated frequency of GBA mutations. GBA-associated PD is characterized by an early onset accompanied by severe cognitive impairment, and "generally these patients suffer more often and more severely from a variety of non-motor symptoms such as neuropsychiatric complaints and autonomic impairment," commented Dr. Elstein.
Gaucher disease is the most common genetic disease affecting Ashkenazi Jewish people who originated primarily from Eastern Europe. According to the National Gaucher Foundation, the disease has an incidence of about 1 in 20,000 live births, rendering it the most prevalent lysosomal storage disorder (a term referring to a group of disorders affecting enzymes that regulate metabolism which are located in cell lysosomes).
For many years, researchers have been investigating whether there are any associations between Parkinson's disease (PD) and lifestyle choices such as smoking and coffee and alcohol consumption. In a review published in the Journal of Parkinson's Disease, the literature concerning alcohol consumption presents conflicting information.
A systematic review of the relevant literature from 2000-2014, from observational studies, found little evidence for either a positive or negative effect on PD risk from alcohol consumption. When weak associations were observed in some reports, the authors found that the studies were at greater risk of selection and recall bias, which could compromise the effects found.
Sixteen articles that met the criteria for inclusion were identified. All were primary research articles, published in English in peer-reviewed journals. These studies had to include a comparison or control group consisting of individuals without PD, report a measure of association between quantity and frequency of alcohol intake and PD risk, and adjust at least for the potential confounding factors of smoking and age. Research that measured alcohol exposure only as drinker versus non-drinker were excluded.
"This review determined several possible methodological weaknesses that could explain the varying and often conflicting results of studies reporting lifestyle exposures such as smoking, coffee/tea and alcohol consumption contributing to PD risk," explained lead investigator Silvana Bettiol, PhD, MPH, School of Medicine, University of Tasmania, Tasmania, Australia. "These included selection or self-selection of controls, difficulties in retrospective assessment of alcohol consumption, differences in the lengths of follow-up periods, and inconsistent definitions of drinkers and non-drinkers."
In addition, in studies in which alcohol consumption and PD incidence were accurately measured over time, only non-significant associations were found, further supporting the argument that various limitations and biases affected many of the studies.
"This study highlights the need for more prospective studies investigating the relationship between alcohol and PD of adequate sample size. Improvements to reporting of studies by investigators particularly with respect to sample size and power would help others interpret the epidemiological significance of any findings," concluded Dr. Bettiol. In summary, "most of the studies proved to be preliminary and improving statistical power to detect joint effects was encouraged."
Okun, a professor in the departments of neurology, neurosurgery and psychiatry, co-directs the UF Center for Movement Disorders and Neurorestoration, which he established with neurosurgeon Kelly Foote, M.D., in 2002. The center, which includes more than 40 interdisciplinary faculty members, delivers personalized care to patients with neurologic disorders such as Parkinson’s disease, Tourette syndrome and dystonia.
Okun has been at the forefront of developing and refining deep brain stimulation, a surgical technique that uses electric pulses delivered to the brain through small implantable leads. The therapy is used to override problematic signals in the brains of patients with movement disorders. Okun also studies a part of the brain called the basal ganglia, and has been developing new device-based approaches for patients suffering from a broad spectrum of neurological diseases. His research is funded by the National Institutes of Health and by many private foundations.
“Dr. Okun has been instrumental at UF in the development of leading-edge research for patients with movement disorders, and he is internationally renowned for his contributions to the field,” said David S. Guzick, M.D., Ph.D., senior vice president for health affairs at UF and president of UF Health. “He has established one of the world’s best deep brain stimulation programs at the University of Florida and, during his time as interim chair, has demonstrated effective leadership in faculty recruitment, residency training and research collaboration, and in creating an overall culture of excellence and commitment.”
Dr. Okun has served as interim chair of the department since January, and his appointment as the department chair comes at a time of major growth and change at UF Health, with a significant focus on the science and practice of neuromedicine. This will be a time in which the large number of neuoroscientists who have been recruited as UF faculty members will be seeking collaborative opportunities with faculty members in the department of neurology. In addition, clinical growth and coordination are anticipated in advance of the 2018 opening of the UF Health Neuromedicine Hospital.
In his capacity as chair, Okun plans to recruit nearly two-dozen new faculty members and to restructure and grow the reputation of the residency program while enhancing its quality. He will work with health system leaders to acquire advanced neuroimaging equipment and help lead UF neurology and neuroscience research programs to national preeminence, according to Good.
“I am truly humbled to be selected as the next UF Health chair of neurology,” Okun said. The construction of the new UF Health Neuromedicine Hospital will be occurring in parallel with important strategic expansions in our faculty and with the expansion of an aggressive research vision. We also plan to enhance our already excellent neurological training programs. The new hospital and the growth of neurology will touch the lives of many people locally and will transform UF into an international destination for those suffering from neurological diseases.”
Okun is the medical adviser for Tyler’s Hope for a Dystonia Cure and the co-chair of the medical advisory board for the Tourette Syndrome Association, and he has been the national medical director for the National Parkinson Foundation for 10 years. Okun was honored at the White House this year as a Champion of Change for Parkinson’s disease.
“Dr. Okun’s involvement in these patient organizations demonstrates the culture of leadership we have at UF Health,” said Ed Jimenez, chief executive officer for UF Health Shands. “With the opening of the UF Health Neuromedicine Hospital in 2018, this leadership will be critical.”
Okun currently holds the Adelaide Lackner professorship in neurology and has published more than 300 peer-reviewed articles. He is author of the bestseller “Parkinson’s Treatment: 10 Secrets to a Happier Life,” the recently released book “10 Breakthrough Therapies for Parkinson’s Disease” and a book of poetry, “Lessons from the Bedside.” He is an associate editor for The New England Journal of Medicine Journal Watch and has served as a reviewer for more than 25 medical journals.
A graduate of the UF College of Medicine, where he also completed an internship and neurology residency, Okun trained at Emory University in basal ganglia physiology and movement disorders surgery. He returned to UF in 2002.
