Posts tagged parkinson's disease
Articles and news from the latest research reports.
Gel reduced daily tremors in Parkinson’s disease
An experimental treatment for Parkinson’s disease reduced by nearly two hours on average the period each day when medication failed to control patients’ slowness and shaking, according to results from a double-blind, phase III clinical trial published in December 2013, in Lancet Neurology.
The study compared AbbVie’s levodopa-carbidopa intestinal gel against the same medication in pill form in patients with advanced disease.
The University of Alabama at Birmingham was among the sites for the study, with David G. Standaert, M.D., Ph.D., chair of the UAB Department of Neurology, an author. Led by the Mount Sinai School of Medicine, preliminary results from the study were first presented at the annual meeting of the American Academy of Neurology in April 2012.
Parkinson’s disease results from the loss of brain cells that make dopamine, which helps to control movement. As dopamine levels fall, patients experience tremors, muscle stiffness and loss of balance. A commonly prescribed treatment, the levodopa-carbidopa combination works as the body converts levodopa into dopamine and carbidopa escorts levodopa to the right part of the brain. The problem is that patients face hours of uncontrolled slowness, freezing and tremors each day — called “off-time” — as the treatment gets into place or wears off.
One reason for the break in treatment coverage is that it comes in a pill, and pills sit in the stomach for up to six hours waiting for it to empty into the small intestine. It is only there that levodopa encounters the proteins capable of transporting it into the bloodstream en route to the brain. Thus, researchers envisioned a system that steadily delivers levodopa gel directly into the small intestine through a surgically placed tube, and with the help of a pump worn on the belt.
“The results are very exciting, considering that other recently approved drugs on the market reduce off-time by, at most, just over an hour,” said Standaert. “In the study, the gel treatment helped patients who had run out of alternatives with current medications. We believe it may be an important new option for patients with severe Parkinson’s, with benefits comparable to more invasive techniques like deep brain stimulation.”
Patients using the gel system saw an average reduction in daily off-time of 1.91 hours, and an increase in “on-time” without troublesome dyskinesia of 1.86 hours compared with the pill form. Nearly all subjects experienced at least one side effect, although most were short-lived and moderate.
(Source: uab.edu)
Among Parkinson’s disease (PD) patients, female, black, and Asian patients are substantially less likely to receive proven deep brain stimulation (DBS) surgery to improve tremors and motor symptoms, according to a new report by a Perelman School of Medicine at the University of Pennsylvania researcher who identified considerable disparities among Medicare recipients receiving DBS for Parkinson’s disease. The study, published in Neurology, found that patients from neighborhoods of lower socioeconomic status were less likely to receive DBS, regardless of race or sex. And patients of minority-serving physician practices were also less likely to receive DBS, irrespective of race. The study demonstrates a need to adjust policy and incentives to provide state of the art care for all Parkinson’s patients.
Parkinson’s disease, a progressive neurodegenerative disease, affects more than 2 million Americans and cannot be prevented or halted. DBS is often prescribed for PD patients when pharmacologic treatments are unable to control involuntary movements or decrease effectiveness over time. While DBS is effective, it requires extensive pre-operative testing, is contraindicated for PD patients who have evidence of cognitive impairment or dementia, and includes out-of-pocket costs that may not be covered by Medicare. DBS out-of-pocket costs average around $2,200 (2007 dollars) per year — 41 percent more than annual non-DBS costs —and would consume approximately 7 percent of the average income in the lowest socioeconomic quartile, potentially limiting the willingness of low-income seniors to consider DBS.
"There are widespread disparities among Parkinson’s patients that are restricting equal utilization of evidence-based care, limiting patients’ quality of life, and increasing societal and health care costs," said lead study author Allison Willis, MD, Assistant Professor of Neurology and of Epidemiology at Penn Medicine. Dr. Willis collaborated on the study with colleagues from Washington University School of Medicine in St. Louis. "Efforts to overcome these disparities, through policy or reimbursement changes, can benefit elders and socioeconomically disadvantaged patients with Parkinson’s disease, as well as other vulnerable groups," said Willis.
Analyzing more than 665,000 Medicare beneficiaries with a Parkinson’s diagnosis between 2007 and 2009 - a decade after DBS was approved for Parkinson’s disease patients - the team identified 8,420 patients treated with DBS (approximately 1 percent). Nearly 95 percent of DBS recipients were white, and 59 percent were male. Hispanic PD patients were nearly equally represented among DBS (2.2 percent of all cases) and non-DBS cases (1.7 percent), whereas black and Asian populations were significantly underrepresented among DBS cases. Black PD patients accounted for 1 percent of DBS cases, and 5.5 percent of non-DBS cases, while less than 1 percent of Asian PD patients received DBS, compared to 1.5 who did not. Women of all races accounted for 41 percent of DBS cases, but 50 percent of non-DBS cases.
Patients with PD of all races who were treated by physicians with the highest concentrations of minority (Asian, Hispanic or black) patients had at least a 15 percent lower likelihood of receiving DBS, compared to providers caring for a small percentage of minority patients. While the data may not account for those who were offered DBS and refused or who were evaluated and did not qualify for DBS, the study suggests that minority-serving providers may be unlikely to perform or refer any of their Medicare beneficiaries with PD for DBS.
In addition, early data suggest that socioeconomic challenges to patients with fixed incomes may also contribute to the treatment disparities. Further research is needed to compare DBS out-of-pocket costs with standard medical and surgical procedures for other conditions.
Penn researchers will continue to study clinical characteristics and progression of disease in minorities and women, to see if they may account for any of the DBS utilization differences. In addition, they hope to look further into physician and practice characteristics along with local medical resources to determine how care differences contribute to disparities in individual DBS use.
Genetic mutation increases risk of Parkinson’s disease from pesticides
A team of researchers has brought new clarity to the picture of how gene-environmental interactions can kill nerve cells that make dopamine. Dopamine is the neurotransmitter that sends messages to the part of the brain that controls movement and coordination. Their discoveries, described in a paper published online in Cell today, include identification of a molecule that protects neurons from pesticide damage.
"For the first time, we have used human stem cells derived from Parkinson’s disease patients to show that a genetic mutation combined with exposure to pesticides creates a ‘double hit’ scenario, producing free radicals in neurons that disable specific molecular pathways that cause nerve-cell death," said Stuart Lipton, M.D., Ph.D., professor and director of Sanford-Burnham Medical Research Institute’s Del E. Webb Center for Neuroscience, Aging, and Stem Cell Research and senior author of the study.
Until now, the link between pesticides and Parkinson’s disease was based mainly on animal studies and epidemiological research that demonstrated an increased risk of disease among farmers, rural populations, and others exposed to agricultural chemicals.
In the new study, Lipton, along with Rajesh Ambasudhan, Ph.D., research assistant professor in the Del E. Webb Center, and Rudolf Jaenisch, M.D., founding member of Whitehead Institute for Biomedical Research and professor of biology at the Massachusetts Institute of Technology, used skin cells from Parkinson’s patients that had a mutation in the gene encoding a protein called alpha-synuclein. Alpha-synuclein is the primary protein found in Lewy bodies—protein clumps that are the pathological hallmark of Parkinson’s disease.
Using patient skin cells, the researchers created human induced pluripotent stem cells (hiPSCs) containing the mutation, and then “corrected” the alpha-synuclein mutation in other cells. Next, they reprogrammed all of these cells to become the specific type of nerve cell that is damaged in Parkinson’s disease, called A9 dopamine-containing neurons—thus creating two sets of neurons—identical in every respect except for the alpha-synuclein mutation.
"Exposing both normal and mutant neurons to pesticides—including paraquat, maneb, and rotenone—created excessive free radicals in cells with the mutation, causing damage to dopamine-containing neurons that led to cell death," said Frank Soldner, M.D., research scientist in Jaenisch’s lab and co-author of the study.
"In fact, we observed the detrimental effects of these pesticides with short exposures to doses well below EPA-accepted levels," said Scott Ryan, Ph.D., researcher in the Del E. Webb Center and lead author of the paper.
Having access to genetically matched neurons with the exception of a single mutation simplified the interpretation of the genetic contribution to pesticide-induced neuronal death. In this case, the researchers were able to pinpoint how cells with the mutation, when exposed to pesticides, disrupt a key mitochondrial pathway—called MEF2C-PGC1alpha—that normally protects neurons that contain dopamine. The free radicals attacked the MEF2C protein, leading to the loss of function of this pathway that would otherwise have protected the nerve cells from the pesticides.
"Once we understood the pathway and the molecules that were altered by the pesticides, we used high-throughput screening to identify molecules that could inhibit the effect of free radicals on the pathway," said Lipton. "One molecule we identified was isoxazole, which protected mutant neurons from cell death induced by the tested pesticides. Since several FDA-approved drugs contain derivatives of isoxazole, our findings may have potential clinical implications for repurposing these drugs to treat Parkinson’s."
While the study clearly shows the relationship between a mutation, the environment, and the damage done to dopamine-containing neurons, it does not exclude other mutations and pathways from being important as well. The team plans to explore additional molecular mechanisms that demonstrate how genes and the environment interact to contribute to Parkinson’s and other neurodegenerative diseases, such as Alzheimer’s and ALS.
"In the future, we anticipate using the knowledge of mutations that predispose an individual to these diseases in order to predict who should avoid a particular environmental exposure. Moreover, we will be able to screen for patients who may benefit from a specific therapy that can prevent, treat, or possibly cure these diseases," Lipton said.
Gene-silencing study finds new targets for Parkinson’s disease
Scientists at the National Institutes of Health have used RNA interference (RNAi) technology to reveal dozens of genes which may represent new therapeutic targets for treating Parkinson’s disease. The findings also may be relevant to several diseases caused by damage to mitochondria, the biological power plants found in cells throughout the body.
"We discovered a network of genes that may regulate the disposal of dysfunctional mitochondria, opening the door to new drug targets for Parkinson’s disease and other disorders," said Richard Youle, Ph.D., an investigator at the National Institute of Neurological Disorders and Stroke (NINDS) and a leader of the study. The findings were published online in Nature. Dr. Youle collaborated with researchers from the National Center for Advancing Translational Sciences (NCATS).
Mitochondria are tubular structures with rounded ends that use oxygen to convert many chemical fuels into adenosine triphosphate, the main energy source that powers cells. Multiple neurological disorders are linked to genes that help regulate the health of mitochondria, including Parkinson’s, and movement diseases such as Charcot-Marie Tooth Syndrome and the ataxias.
Some cases of Parkinson’s disease have been linked to mutations in the gene that codes for parkin, a protein that normally roams inside cells, and tags damaged mitochondria as waste. The damaged mitochondria are then degraded by cells’ lysosomes, which serve as a biological trash disposal system. Known mutations in parkin prevent tagging, resulting in accumulation of unhealthy mitochondria in the body.
RNAi is a natural process occurring in cells that helps regulate genes. Since its discovery in 1998, scientists have used RNAi as a tool to investigate gene function and their involvement in health and disease.
Dr. Youle and his colleagues worked with Scott Martin, Ph.D., a coauthor of the paper and an NCATS researcher who is in charge of NIH’s RNAi facility. The RNAi group used robotics to introduce small interfering RNAs (siRNAs) into human cells to individually turn off nearly 22,000 genes. They then used automated microscopy to examine how silencing each gene affected the ability of parkin to tag mitochondria.
"One of NCATS’ goals is to develop, leverage and improve innovative technologies, such as RNAi screening, which is used in collaborations across NIH to increase our knowledge of gene function in the context of human disease," said Dr. Martin.
For this study, the researchers used RNAi to screen human cells to identify genes that help parkin tag damaged mitochondria. They found that at least four genes, called TOMM7, HSPAI1L, BAG4 and SIAH3, may act as helpers. Turning off some genes, such as TOMM7 and HSPAI1L, inhibited parkin tagging whereas switching off other genes, including BAG4 and SIAH3, enhanced tagging. Previous studies showed that many of the genes encode proteins that are found in mitochondria or help regulate a process called ubiquitination, which controls protein levels in cells.
Next the researchers tested one of the genes in human nerve cells. The researchers used a process called induced pluripotent stem cell technology to create the cells from human skin. Turning off the TOMM7 gene in nerve cells also appeared to inhibit tagging of mitochondria. Further experiments supported the idea that these genes may be new targets for treating neurological disorders.
"These genes work like quality control agents in a variety of cell types, including neurons," said Dr. Youle. "The identification of these helper genes provides the research community with new information that may improve our understanding of Parkinson’s disease and other neurological disorders."
The RNAi screening data from this study are available in NIH’s public database, PubChem, which any researcher may analyze for additional information about the role of dysfunctional mitochondria in neurological disorders.
"This study shows how the latest high-throughput genetic technologies can rapidly reveal insights into fundamental disease mechanisms," said Story Landis, Ph.D., director of the NINDS. "We hope the results will help scientists around the world find new treatments for these devastating disorders."
Symptoms of Parkinson’s Disease Linked to Fungus
Scientists at Rutgers and Emory universities have discovered that a compound often emitted by mold may be linked to symptoms of Parkinson’s disease.
Arati Inamdar and Joan Bennett, researchers in the School of Environmental and Biological Sciences at Rutgers, used fruit flies to establish the connection between the compound – popularly known as mushroom alcohol – and the malfunction of two genes involved in the packaging and transport of dopamine, the chemical released by nerve cells to send messages to other nerve cells in the brain.
The findings were published online today in the Proceedings of the National Academy of Sciences.
“Parkinson’s has been linked to exposure to environmental toxins, but the toxins were man-made chemicals,” Inamdar said. “In this paper, we show that biologic compounds have the potential to damage dopamine and cause Parkinson’s symptoms.”
For co-author Bennett, the research was more than academic. Bennett was working at Tulane University in New Orleans when Hurricane Katrina struck the Gulf Coast in 2005. Her flooded house became infested with molds, which she collected in samples, wearing a mask, gloves and protective gear.
“I felt horrible – headaches, dizziness, nausea,” said Bennett, now a professor of plant pathology and biology at Rutgers. “I knew something about ‘sick building syndrome’ but until then I didn’t believe in it. I didn’t think it would be possible to breathe in enough mold spores to get sick.” That is when she formed her hypothesis that volatiles might be involved.
Inamdar, who uses fruit flies in her research, and Bennett began their study shortly after Bennett arrived at Rutgers. Bennett wanted to understand the connection between molds and symptoms like those she had experienced following Katrina.
The scientists discovered that the volatile organic compound 1-octen-3-ol, otherwise known as mushroom alcohol, can cause movement disorders in flies, similar to those observed in the presence of pesticides, such as paraquat and rotenone. Further, they discovered that it attacked two genes that deal with dopamine, degenerating the neurons and causing the Parkinson’s-like symptoms.
Studies indicate that Parkinson’s disease – a progressive disease of the nervous system marked by tremor, muscular rigidity and slow, imprecise movement — is increasing in rural areas, where it’s usually attributed to pesticide exposure. But rural environments also have a lot of mold and mushroom exposure.
“Our work suggests that 1-octen-3-ol might also be connected to the disease, particularly for people with a genetic susceptibility to it,” Inamdar said. “We’ve given the epidemiologists some new avenues to explore.”
(Source: news.rutgers.edu)
Simple Dot Test May Help Gauge the Progression of Dopamine Loss in Parkinson’s Disease
A pilot study by a multi-disciplinary team of investigators at Georgetown University suggests that a simple dot test could help doctors gauge the extent of dopamine loss in individuals with Parkinson’s disease (PD). Their study is being presented at Neuroscience 2013, the annual meeting of the Society for Neuroscience.
“It is very difficult now to assess the extent of dopamine loss — a hallmark of Parkinson’s disease — in people with the disease,” says lead author Katherine R. Gamble, a psychology PhD student working with two Georgetown psychologists, a psychiatrist and a neurologist. “Use of this test, called the Triplets Learning Task (TLT), may provide some help for physicians who treat people with Parkinson’s disease, but we still have much work to do to better understand its utility,” she adds.
Gamble works in the Cognitive Aging Laboratory, led by the study’s senior investigator, Darlene Howard, PhD, Davis Family Distinguished Professor in the department of psychology and member of the Georgetown Center for Brain Plasticity and Recovery.
The TLT tests implicit learning, a type of learning that occurs without awareness or intent, which relies on the caudate nucleus, an area of the brain affected by loss of dopamine.
The test is a sequential learning task that does not require complex motor skills, which tend to decline in people with PD. In the TLT, participants see four open circles, see two red dots appear, and are asked to respond when they see a green dot appear. Unbeknownst to them, the location of the first red dot predicts the location of the green target. Participants learn implicitly where the green target will appear, and they become faster and more accurate in their responses.
Previous studies have shown that the caudate region in the brain underlies implicit learning. In the study, PD participants implicitly learned the dot pattern with training, but a loss of dopamine appears to negatively impact that learning compared to healthy older adults.
“Their performance began to decline toward the end of training, suggesting that people with Parkinson’s disease lack the neural resources in the caudate, such as dopamine, to complete the learning task,” says Gamble.
In this study of 27 people with PD, the research team is now testing how implicit learning may differ by different PD stages and drug doses.
“This work is important in that it may be a non-invasive way to evaluate the level of dopamine deficiency in PD patients, and which may lead to future ways to improve clinical treatment of PD patients,” explains Steven E. Lo, MD, associate professor of neurology at Georgetown University Medical Center, and a co-author of the study.
They hope the TLT may one day be a tool to help determine levels of dopamine loss in PD.
(Source: explore.georgetown.edu)
Lasers might be the cure for brain diseases such as Alzheimer’s and Parkinson’s
Researchers at Chalmers University of Technology in Sweden, together with researchers at the Polish Wroclaw University of Technology, have made a discovery that may lead to the curing of diseases such as Alzheimer’s, Parkinson’s and Creutzfeldt-Jakob disease (the so called mad cow disease) through photo therapy.
The researchers discovery, which was published yesterday in the journal Nature Photonics, is that it is possible to distinguish aggregations of the proteins, believed to cause the diseases, from the the well-functioning proteins in the body by using multi-photon laser technique.
“Nobody has talked about using only light to treat these diseases until now. This is a totally new approach and we believe that this might become a breakthrough in the research of diseases such as Alzheimer’s, Parkinson’s and Creutzfeldt-Jakob disease. We have found a totally new way of discovering these structures using just laser light”, says Piotr Hanczyc at Chalmers University of Technology.
If the protein aggregates are removed, the disease is in principle cured. The problem until now has been to detect and remove the aggregates.
The researchers now harbor high hopes that photo acoustic therapy, which is already used for tomography, may be used to remove the malfunctioning proteins. Today amyloid protein aggregates are treated with chemicals, both for detection as well as removal. These chemicals are highly toxic and harmful for those treated.
With multi photon laser the chemical treatment would be unnecessary. Nor would surgery be necessary for removing of aggregates. Due to this discovery it might, thus, be possible to remove the harmful protein without touching the surrounding tissue.
These diseases arise when amyloid beta protein are aggregated in large doses so they start to inhibit proper cellular processes.
Different proteins create different kinds of amyloids, but they generally have the same structure. This makes them different from the well-functioning proteins in the body, which can now be shown by multi photon laser technique.
Two forms of Parkinson’s disease identified
Why can the symptoms of Parkinson’s disease vary so greatly from one patient to another? A consortium of researchers, headed by a team from the Laboratoire CNRS d’Enzymologie et Biochimie Structurales, is well on the way to providing an explanation. Parkinson’s disease is caused by a protein known as alpha-synuclein, which forms aggregates within neurons, killing them eventually. The researchers have succeeded in characterizing and producing two different types of alpha-synuclein aggregates. Better still, they have shown that one of these two forms is much more toxic than the other and has a greater capacity to invade neurons. This discovery takes account, at the molecular scale, of the existence of alpha-synuclein accumulation profiles that differ from one patient to the next. These results, published on October 10 in Nature Communications, represent a notable advance in our understanding of Parkinson’s disease and pave the way for the development of specific therapies targeting each form of the disease.
Parkinson’s disease, which is the second most frequent neurodegenerative disease after Alzheimer’s, affects some 150,000 people in France. According to those suffering from the disease, it can manifest itself in the form of uncontrollable shaking (in 60% of patients) or by less-localized symptoms such as depression, behavioral and motor disorders. These differences in symptoms point to different forms of Parkinson’s disease.
This condition, for which no curative treatment currently exists, is caused by the aggregation in the form of fibrillar deposits of alpha-synuclein, a protein that is naturally abundant at neuron junctions. These misfolded alpha-synuclein aggregates propagate between neurons. When they invade a new neuron, they are capable of recruiting normal alpha-synuclein and adding it to the deposit. For this reason, many researchers advocate that the alpha-synuclein of the aggregates should be considered as an infectious protein, in other words a prion. Highly toxic, the alpha-synuclein deposits end up by triggering a process of apoptosis, i.e. cell death.
The researchers have shown that there is not just one single type of aggregate. They succeeded in producing two types of aggregate that only differ in how the protein stacks up. At the millionth of a millimeter scale, the first form of aggregate resembles spaghetti, whereas the second form is long and flat, recalling the shape of wider pasta such as linguine. The team of scientists then tried to determine whether these structural differences result in functional differences. To find out, they placed the two types of aggregates in contact with neuronal cells in culture. They discovered that the capacity of the “spaghetti” form to bind to and penetrate cells is notably greater than that of the “linguine” form. The “spaghetti” form is also considerably more toxic and rapidly kills the infected cells. This form has shown itself to be capable of resisting the cell mechanisms responsible for eliminating it, whereas the “linguine” form is, to a certain extent, controlled by the cell.
The researchers are convinced that the existence of at least two forms of alpha-synuclein aggregates explains why doctors are faced with different Parkinson’s diseases depending on the patient. Experiments on mice are currently underway to confirm this hypothesis. Furthermore, the scientists consider that analysis of the type of aggregate could lead to an efficient diagnosis method, which would make it possible in particular to assess the virulence of the disease for each patient. Finally, they hope that by refining the characterization of the structure of the aggregates, it will be possible to develop targeted therapeutic strategies for each variant in order to slow down the propagation of abnormal alpha-synuclein within the brain.
Study Identifies Possible Biomarker for Parkinson’s Disease
Researchers discover that an important clue to diagnosing Parkinson’s disease may lie just beneath the skin
Although Parkinson’s disease is the second most prevalent neurodegenerative disorder in the U.S., there are no standard clinical tests available to identify this widespread condition. As a result, Parkinson’s disease often goes unrecognized until late in its progression, when the brain’s affected neurons have already been destroyed and telltale motor symptoms such as tremor and rigidity have already appeared.
Now researchers from Beth Israel Deaconess Medical Center (BIDMC) have discovered that an important clue to diagnosing Parkinson’s may lie just beneath the skin.
In a study scheduled to appear in the October 29 print issue of the journal Neurology and currently published on-line, the investigators report that elevated levels of a protein called alpha-synuclein can be detected in the skin of Parkinson’s patients, findings that offer a possible biomarker to enable clinicians to identify and diagnose PD before the disease has reached an advanced stage.
Parkinson’s disease affects more than 1 million individuals throughout the U.S. Diagnosis is currently made through neurological history and examination, often by a patient’s primary care physician.
“Even the experts are wrong in diagnosing Parkinson’s disease a large percentage of the time,” says senior author Roy Freeman, MD, Director of the Autonomic and Peripheral Nerve Laboratory at BIDMC and Professor of Neurology at Harvard Medical School. “A reliable biomarker could help doctors in more accurately diagnosing Parkinson’s disease at an earlier stage and thereby offer patients therapies before the disease has progressed.”
Alpha-synuclein is a protein found throughout the nervous system. Although its function is unknown, it is the primary component of protein clumps known as Lewy bodies, which are considered the hallmark of Parkinson’s disease. There is accumulating evidence that the protein plays a role in Parkinson’s disease development.
“Alpha-synuclein deposition occurs early in the course of Parkinson’s disease and precedes the onset of clinical symptoms,” explains Freeman, who with his coauthors suspected that the protein was elevated in the skin’s structures with autonomic innervation.
“Symptoms related to the autonomic nervous system, including changes in bowel function, temperature regulation, and blood pressure control may antedate motor symptoms in Parkinson’s patients,” he explains. “Skin-related autonomic manifestations, including excessive and diminished sweating and changes in skin color and temperature, occur in almost two-thirds of patients with Parkinson’s disease. The skin can provide an accessible window to the nervous system and based on these clinical observations, we decided to test whether examination of the nerves in a skin biopsy could be used to identify a PD biomarker.”
To test this hypothesis, the research team enrolled 20 patients with Parkinson’s disease and 14 control subjects of similar age and gender. The participants underwent examinations, autonomic testing and skin biopsies in three locations on the leg. Alpha-synuclein deposition and density of cutaneous sensory, sudomotor and pilomotor nerve fibers were measured.
As predicted, their results showed that alpha-synuclein was increased in the cutaneous nerves supplying the sweat glands and pilomotor muscles in the Parkinson’s patients. Higher alpha-synuclein deposition in the nerves supplying the skin’s autonomic structures was associated with more advanced Parkinson’s disease and worsening autonomic function.
“There is a strong and unmet need for a biomarker for Parkinson’s disease,” says Freeman. “Alpha-synuclein deposition within the skin has the potential to provide a safe, accessible and repeatable biomarker. Our next steps will be to test whether this protein is present in the cutaneous nerves of individuals at risk for Parkinson’s disease, and whether measurement of alpha-synuclein deposition in the skin can differentiate Parkinson’s disease from other neurodegenerative disorders.”
(Source: newswise.com)
Small brain biopsies can be used to grow large numbers of patient’s own brain cells
A group of really brainy scientists have moved closer to growing “therapeutic” brain cells in the laboratory that can be re-integrated back into patients’ brains to treat a wide range of neurological conditions. According to new research published online in The FASEB Journal, brain cells from a small biopsy can be used to grow large numbers of new personalized cells that are not only “healthy,” but also possess powerful attributes to preserve and protect the brain from future injury, toxins and diseases. Scientists are hopeful that ultimately these cells could be transformed in the laboratory to yield specific cell types needed for a particular treatment, or to cross the “blood-brain barrier” by expressing specific therapeutic agents that are released directly into the brain.
"This work is an example of how integrating basic science and clinical care may reveal privileged opportunities for biomedical research," said Matthew O. Hebb, M.D., Ph.D., FRCSC, a researcher involved in the work from the Departments of Clinical Neurological Sciences (Neurosurgery), Oncology and Otolaryngology at the University of Western Ontario in Ontario, Canada. "It is our hope that the results of this study provide a footing for further advancement of personalized, cell-based treatments for currently incurable and devastating neurological disorders."
Scientists enrolled patients with Parkinson’s disease who were scheduled to have deep brain stimulation (DBS) surgery, a commonly used procedure that involves placing electrodes into the brain. Before the electrodes were implanted, small biopsies were removed near the surface of the brain and multiplied in culture to generate millions of patient-specific cells that were then subjected to genetic analysis. These cells were complex in their make-up, but exhibited regeneration and characteristics of a fundamental class of brain cells, called glia. They expressed a broad array of natural and potent protective agents, called neurotrophic factors.
"From an extremely small amount of brain tissue, we will one day be able to do very big things," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. “For centuries, treating the brain effectively and safely has been elusive. This advance opens the doors to not only new therapies for a myriad of brain diseases, but new ways of delivering therapies as well.”
(Source: eurekalert.org)