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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 have Parkinson's
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Saturday, December 26, 2015

In Parkinson’s Disease Patients, Brain Cells Lose Their ‘Powerhouses’

Dec. 25, 2015
The brain cells of patients with Parkinson’s disease undergo a shutdown of their energy powerhouses, the mitochondria, according to a new study. Because this shutdown probably occurs early in Parkinson’s cases, the finding could lead to therapies that stop the disease before too much damage has been done.Researchers identified 10 groups of genes called gene sets, each carrying out one biological process associated with Parkinson’s disease. Many of these gene sets are involved in helping the mitochondria do their job. Even in people whose autopsies revealed early Parkinson’s who did not have clinical symptoms, but whose brains showed signs of the disease these gene sets were not expressed properly, meaning the mitochondria in those cells probably weren’t working.
The loss of working mitochondria, which produce most of the cell’s energy, may contribute to the onset of the disease, the researchers said.
All of these gene sets are controlled by a single gene, a “master regulator” called PGC-1alpha that switches the gene sets on or off. This gene could be a target for future therapies to treat or prevent the disease, the researchers said.
Their results are published today (Oct. 6) in the journal Science Translational Medicine.
Parkinson’s genes
Parkinson’s affects about 5 million people globally. The disease kills brain cells that produce the chemical dopamine. This impairs patients’ movements, causing symptoms such as tremors, muscle stiffness and impaired balance and coordination. The cause of the disease is not known.Clemens Scherzer, of Brigham and Women’s Hospital and Harvard Medical School, and his colleagues analyzed genetic data from 17 studies involving a total of 322 human brain tissue samples and 88 blood samples. Of these, 185 were derived from the dopamine-producing brain cells of deceased patients with Parkinson’s.
They initially found 28 gene sets to be associated with Parkinson’s. Further research looking into the genomes of patients with early Parkinson’s narrowed the field to 10 gene sets.
Some of these gene sets contain the genetic code to make proteins involved in the electron transport chain a set of reactions inside the mitochondria that produce energy. Defects in the electron transport chain would severely affect the ability of the brain cells to generate energy, the researchers said.
It’s possible that genetic and environmental influences , along with aging, have a combined impact on the expression of the mitochondrial genes, Scherzer said.
Future drugs
Medications that activate the PGC-1alpha gene already have been approved by the U.S. Food and Drug Administration for treatment of other diseases, such as diabetes . This means pharmaceutical companies may be able to develop new drugs for Parkinson’s by tweaking already developed drugs rather than by starting from scratch, the researchers said.
The study was funded by the National Institute of Neurological Disorders and Stroke, the National Institute on Aging, and the Michael J. Fox Foundation, among others.sources

What it feels like to have Parkinson’s disease

In 1985, science journalist Jon Palfreman investigated a group of drug addicts who were struck with Parkinson’s-like symptoms after taking tainted heroin.
Thirty years later, Palfreman was diagnosed with Parkinson’s disease himself. His book, “Brain Storms,” describes his journey with the disease and new treatments for patients.
“Initially I denied [my diagnosis] and sought second opinions. I got pretty angry. I tried to keep it secret for a while, just like Michael J. Fox did,” Palfreman says, “It took me, I’d say, about a year before I really processed it properly and then I realized that I had a destiny to use my training as a science journalist and my insights as a patient to explore this malady, which was now going to be part of my life.”About 60,000 people each year in the US alone are diagnosed with Parkinson’s disease. Palfreman says the malady means many things that he used to do automatically, now come with much more difficulty.

“It is very much like getting on a plane and going to London and renting a car. You can drive on the left-hand side of the road, but you have to use your conscious brain to pay attention. Everything’s a bit harder. When I walk, I have to sort of consciously move my arms back and forth. Whereas, when a healthy person does it, it’s automatic. And so a lot of things that you got for free you have to work at,” Palfreman says.

The disease has three stages. The first noticeable symptoms are subtle, such as a loss of smell, constipation and possible sleeping disorders. After that, the disease attacks a person’s ability to move. The third stage produces cognitive impairment and hallucinations.
“What we classically think of Parkinson’s — the tremor, the slowness, the rigidity, the stooped gait — is really the middle act of a three-act play and that, basically, the diseases present maybe 10 or 15 years before a person gets diagnosed,” Palfreman says. “It’s a much more systemic disease than it was once thought to be.”There are several new treatments for the disease Palfreman has been watching. One of them is based on the theory that the disease is caused by a protein, alpha-synuclein, going rogue, forming clumps called amyloids, and jumping from cell to cell, killing cells in their wake.
“If alpha-synuclein is causing all the problems, then trying to reduce the levels of it makes perfect sense, and in the next year or two, going into clinical trials, there are a number of products which are designed to sort of dissolve alpha-synuclein,” Palfreman says. “If they work, I mean the prospects are amazing. Somebody who didn’t have the disease, if you can get in early enough, would never develop the motor symptoms. And somebody like me who had the motor symptoms could possibly be stabilized so it didn’t get any worse. So there’s a lot of excitement at the moment around this.”
Palfreman says there are other things people with Parkinson’s can do to control the disease.

“The one thing which really everybody should do is regular exercise because people who do exercise and stay mobile, they do much, much, much better than people who withdraw or give up,” Palfreman says. “Because you’ve still got the conscious part of your brain, you can still drive like you’re driving into London on the wrong side of the road. It just takes a bit more energy and effort, but it still works.”

In the future, Palfreman predicts medical specialists will develop more advanced ways to control the disease.
“Just like we have very sophisticated heart pacemakers, we might get a situation where I might get an electrode in my brain and, just before my my left hand wants to set off a tremor it sets off a pulse and reboots that part of the brain. And I think these things are pretty promising so that even if you haven’t got a total cure, the management thing will become much better and we’ll be able to live pretty much essentially normal lives.”

Thursday, December 24, 2015

Hepatitis C Linked to Parkinson's Disease

Pauline Anderson

December 23, 2015
Infection with the hepatitis C virus (HCV) significantly increases the risk for Parkinson's disease (PD), new research shows.
"The risk of developing PD is obviously multifactorial, and our study shows that hepatitis C virus infection can be one of the risk factors," said lead investigator Hsin-Hsi Tsai, MD, Neurology Department, National Taiwan University Hospital, Taipei.
The positive association between HCV infection and PD has clinical implications in high endemic HCV areas such as Taiwan, said Dr Tsai. "More detailed neurological tests and functional images might help us detect early PD in anti-HCV–positive patients."

Possible Mechanism
In most cases, exposure to HCV, a small, enveloped RNA virus, leads to chronic infection, causing progressive liver disease, including hepatic fibrosis, cirrhosis, and hepatocellular carcinoma.
In developed countries, HCV is transmitted largely by injection from illicit drug use. In Taiwan, a history of blood transfusion is the most important risk factor for the HCV infection, according to the authors. That country has a prevalence of anti-HCV seropositivity of about 5%.
For the study, researchers used the National Health Insurance Program, a mandatory single-payer program covering more than 99% of Taiwan residents, and the Longitudinal Health Insurance Database, which houses information on 1 million persons randomly selected from the National Health Insurance database.
The analysis included 49,967 patients with viral hepatitis: 35,619 (71.3%) with hepatitis B virus (HBV) infection, 10,286 (20.6%) with HCV infection, and 4062 (8.1%) with both infections.
The mean age of the patients was about 46 years, and 43.5% of patients were women. Patients were followed for 12 years.
The investigators found a 2.5-fold increased risk for PD in patients with HCV infection compared with controls (no HCV or HBV) (hazard ratio [HR], 2.5; 95% confidence interval [CI], 2.07 - 3.02).
After adjustment for age, sex, and comorbidities, including hyperlipidemia, hypertension, ischemic heart disease, epilepsy diabetes, cirrhosis, stroke, and head injury, the association between HCV and PD remained statistically significant (adjusted HR, 1.29; 95% CI, 1.06 - 1.56; P < .05).
The adjusted HRs for HBV and coinfection were not statistically significant. However, the authors pointed out that there were too few patients with PD in the "both" category to attain statistical significance.
An analysis stratified by age, sex, or comorbidity found that a positive association between HCV and PD was maintained in patients under age 65 years, men, or those with a combination of any of the comorbidities. Being male and having comorbidities could represent "hits" in the "second hit" theory of PD.
The theory, she said, is that HCV enters the central nervous system (CNS) by disrupting the integrity of the blood-brain barrier, altering dopaminergic neuronal transmission in the midbrain, and triggering neuro-inflammation, which results in neuronal damage. This damage could be the first "hit," with second "hits" possibly including age, male sex, other environmental exposures (such as pesticides), and head injury.The link between HCV infection and PD is supported by findings that this infection might release inflammatory cytokines, such as sICAM-1 and RANTES signaling, which may play a role in the pathogenesis of PD, said Dr Tsai.
Dementia Link
HCV infection has also been linked to dementia, another neurodegenerative disease. Although the mechanisms here are not well understood, it's believed that a similar pathogenesis may be at play, said Dr Tsai.
In contrast to HCV, there is no evidence that HBV, which belongs to the Hepadnaviridae family, is neuroinvasive. An earlier study on rats by Dr Tsai and colleagues showed that HBV does not induce dopaminergic neuronal toxicity.
But other viruses have been linked to PD. One of the best-known examples is the type A H1N1 influenza virus that caused the 1918 influenza pandemic.
"It has been shown that people born during the time of the pandemic influenza outbreak of 1918 have a 2- to 3-fold increased risk of Parkinson's disease than those born prior to 1888 or after 1924," Dr Tsai told Medscape Medical News.
Another example is HIV, the retrovirus that causes AIDS. HIV can quickly infect astrocyte and microglia (monocytic lineage), causing CNS involvement, said Dr Tsai. "It has been reported that 5% to 50% of all AIDS patients have some motor dysfunction, such as bradykinesia, cogwheel rigidity, and tremor."Several other viruses, including Coxsackie, Japanese encephalitis B, western equine encephalitis, and herpes, may also be linked to parkinsonism.
A limitation of the study was that it used healthcare codes to identify PD and viral hepatitis instead of clinical assessment, laboratory data, or neuroimaging. In addition, the database the authors used doesn't contain information on the duration of viral hepatitis and some HCV risk factors.
"Unfortunately, we were unable to investigate the association between IV [intravenous] drug users and HCV infection in the current study because there were no data regarding the use of illicit drug or associated behaviors" in the database that was used, said Dr Tsai.
Interpret With Caution
Reached for a comment, Michael S. Okun, MD, chairman, University of Florida Health Neurology, Gainesville, and national medical director, National Parkinson Foundation, said the idea that viruses such as HCV can cross the blood-brain barrier, cause inflammation, and lead to death of cells important to PD isn't new.
"However, this study is one of the few to offer well-documented evidence of at least an association," said Dr Okun. One of the strengths of the study, he noted, is its large sample size.
Nevertheless, because of the lack of diagnostic certainty of PD and the missing details, such as transfusion history and drug abuse, the results must be interpreted cautiously, he said.
"This study should be easily reproduced by data from other countries, and we look forward to verification of the result."
For clinicians, the new information should make them more aware that HCV may be a risk factor for the later development of PD, added Dr Okun. "The threshold for ordering a neurological consultation in HCV cases should be lower."
He noted that the authors didn't explore whether treatment for HCV infection could change the risk.
Also commenting on the findings for Medscape Medical News, Beth Vernaleo, PhD, associate director of research programs, Parkinson's Disease Foundation, said, "the epidemiological study builds upon previous lab research that identifies hepatitis C as a possible risk factor for Parkinson's. There's no cause for alarm for individuals with hepatitis C — for most people, several risk factors must be present for Parkinson's to develop. But we are hopeful that these results will spur additional studies to understand brain changes that might underlie both diseases, which in turn may advance research and treatments in the future."
The authors and Dr Okun have disclosed no relevant financial relationships.
Neurology. Published online December 23, 2015. Abstract

Wednesday, December 23, 2015

‘Gunslinger’s gait’ should be included in differential diagnosis

By Eleanor McDermid, Senior medwireNews Reporter
Published on December 23, 2015

An analysis of the gait of top Russian officials has led researchers to warn neurologists against interpreting a probable behavioural adaptation as a pathological gait pattern.

As reported in the Christmas edition of TheBMJ, Bastiaan Bloem (Radboud University Medical Centre, Nijmegen, the Netherlands) and colleagues noted that five Russian officials, including President Vladimir Putin, all have a markedly reduced right-arm swing when walking.

Studying YouTube videos, the team found multiple examples of reduced right-arm swing in these officials, along with evidence of otherwise normal function of the right arm.

They highlight that much of their evidence came from ceremonial events, in which the officials took long walks along red carpets.
“We always tell our neurology residents that one cannot adequately assess gait (and especially arm swing) in the limited confines of the consulting room and urge them to take their patients out into the corridor”, they say.
Assuming that all five Russian officials were not, in fact, presenting early signs of Parkinson’s disease, Bloem and team uncovered an alternative explanation, in a KGB manual advising trainees to keep their right arm close to their chest when walking, to facilitate rapid access to their firearm.

They therefore suggest that the reduced right-arm swing is a behavioural adaptation, which they term “gunslinger’s gait”. Two of the Russian officials, including Putin, are former KGB officials and two others have strong links to the Russian military, suggesting that all four could have received firearms training. The fifth official has no known links, so the team suggests his reduced arm swing could be a different type of behavioural adaptation: “the ‘imitate the boss’ phenomenon”.

“We conclude that unawareness of weaponry training might lead clinicians to misdiagnose healthy individuals as having a pathological gait, perhaps even parkinsonian”, say the researchers.

“We recommend that neurologists, in particular those working in Russia, include ‘gunslinger’s gait’ in their differential diagnosis of an asymmetrically reduced arm swing, along with other known causes such as Parkinson’s disease and shoulder pathology.”

Licensed from medwireNews with permission from Springer Healthcare Ltd. ©Springer Healthcare Ltd. All rights reserved. Neither of these parties endorse or recommend any commercial products, services, or equipment.

Opicapone simplifies levodopa-related motor fluctuation treatment

Published on December 23, 2015

Once-daily opicapone is effective for the treatment of end-of-dose motor fluctuations in patients receiving levodopa for Parkinson’s disease, phase III study findings show.
The results indicate that at a dose of 50 mg/day the drug, a potent third-generation catechol-O-methyltransferase (COMT) inhibitor, was superior to placebo and non-inferior to entacapone (200 mg with each levodopa dose) in reducing the absolute time patients spent in the off state.
The magnitude of effect with opicapone was greater that than of entacapone, with a 26.2 minute greater reduction in the time spent in the off state after 14–15 weeks of treatment and a 60.8 minute greater reduction compared with placebo.
Opicapone 50 mg “is, therefore, the only once-daily COMT inhibitor to provide a mean reduction in time in the off state that is clinically relevant,” say Patrício Soares-da-Silva (BIAL, Coronado, Portugal) and team.
The average changes from baseline in time spent in the off state over a 24-hour period were 116.8 minutes in 115 patients taking opicapone 50 mg/day, 96.3 minutes in 120 patients taking entacapone and 56.0 minutes in the placebo group.
Opicapone 25 mg and 5 mg were also tested in 116 and 119 patients, respectively, but the effects of these doses on the time patients spent in the off state did not differ significantly from that of placebo.
The researchers note in The Lancet Neurology that, in addition to greater reductions in the time patients spent in the off state, opicapone 50 mg was associated with greater increases in the percentage of time patients spent in the on state without troublesome dyskinesia, with a 5.4% difference compared with placebo and a 1.2% difference compared with entacapone.
Improvements in global symptoms were seen in significantly more patients taking opicapone 50 mg than in those taking entacapone, and while numerical improvements in motor symptom scores were seen in all groups, differences between active treatment and placebo groups were not significant.

Dyskinesia was the most common treatment-emergent adverse event and, in line with its more potent inhibition of COMT, occurred most frequently in patients taking opicapone 50 mg.
Otherwise, the incidence of serious treatment-emergent adverse events did not differ significantly from that in the placebo or entacapone group.
Soares-da-Silva and colleagues believe that “[o]picapone once daily could enable a simplified drug regimen that allows the physician to individually tailor the existing levodopa daily regimen by potentially decreasing the total daily levodopa dose, increasing the dosing interval, and ultimately reducing the number of intakes, therefore maximising its benefit.”
Commentators David Devos and Caroline Moreau, from the University of Lille in France, agree that “[t]hese clinical trial results are likely to substantially affect clinical practice”.
And add that some key questions now need to be addressed, including whether administration of opicapone in the early stages of levodopa therapy could delay the onset of motor complications and whether a patient’s COMT genotype could influence the drug dose.

medwireNews ( is an independent clinical news service provided by Springer Healthcare Limited. © Springer Healthcare Ltd; 2015
Licensed from medwireNews with permission from Springer Healthcare Ltd. ©Springer Healthcare Ltd. All rights reserved. Neither of these parties endorse or recommend any commercial products, services, or equipment.

Researchers, patients trade new insights at International Dementia with Lewy Bodies Conference

23 Dec 2015

You thought Alzheimer's was complicated? Or Parkinson's? Try dementia with Lewy bodies, the disease occupying the awkward territory between those two poles. DLB is arguably the second-most-common form of dementia, but it is heterogeneous and often overlooked.

Yet the International Dementia with Lewy Bodies Conference held earlier this month in Fort Lauderdale, Florida, showcased a field coming into its own. For four days, 400 researchers, patients, care partners, and other stakeholders traded new insights. Because this conference last convened about a decade ago, there was much to learn. Over the din of disease classification debates that perennially accompany spectrum diseases, the meeting reflected a field trying to build on a broadly accepted consensus diagnosis, its unifying foundation.

Pharmaceutical companies are dipping in their toes, brain imaging is making it possible to see what's going on in the brain, GWAS are ramping up, and prodromal biomarker cohorts are forming. Farthest ahead is Japan—the only country that has annual DLB conferences, an approved medication, as well as arguably the best diagnostic scan standardized across centers. Read Alzforum's six-part daily news series about DLB, starting today.

Bern study sheds light on the brain mechanism of arousal

Published on December 22, 2015 

Scientists from Bern have discovered a mechanism which is responsible for the rapid arousal from sleep and anesthesia in the brain. The results of their study suggest new strategies for the medical treatment of sleep disorders and recovery of consciousness in vegetative states.
Chronic sleep perturbances affect 10-20% of the population of Switzerland and almost everyone experiences sleep problems at least once in a lifetime. Beside the quantity of sleep that is often affected in insomnia, clinical and experimental studies emphasize that the quality of sleep (e.g., depth of  your sleep) is equally important for a good night's sleep and a complete recovery of «body and mind» functions. «The consequences of sleep perturbations on life quality go far beyond daytime sleepiness and mood alteration. Cognitive impairment, hormonal imbalance and high susceptibility to cardiac or metabolic disorders are amongst some of the negative impacts frequently associated with subtle chronic sleep problems», says Prof. Antoine Adamantidis from the Department of Clinical Research of the University of Bern and Department of Neurology at the Bern University Hospital.
The quantity and the quality of sleep are now considered as an early marker of many neurological disorders including Alzheimer's disease, Parkinson's disease, and schizophrenia. Unfortunately, pharmaceutical strategies combined with improved life hygiene have limited effect. «Personalized medicine» strategies for the treatment of either insufficient sleep quality or quantity are missing.
Brain circuits for arousal and consciousness
Therefore, intensive experimental research is conducted to understand how brain circuits control sleep-wake cycle and consciousness - an enigma in modern Neurosciences and an exciting key mystery to resolve. Together with fellow researcher Carolina Gutierrez Herrera and colleagues from Germany, Adamantidis made a dual discovery: his team identified a new circuit in the brain of mice whose activation causes rapid wakefulness while its inhibition deepens sleep. The study was published in the scientific journal «Nature Neuroscience».
Mammalian sleep is classically divided in two phases, including non-rapid eye movement (NREM) sleep or «light» sleep, and REM (or paradoxical) sleep or «deep»/dreaming sleep. Key brain circuits for those two states have been identified.,However, the precise underlying mechanisms - such as the onset, maintenance and termination of sleep and dreaming - remain unknown.

Adamantidis and Gutierrez Herrera identified a new neural circuit between two brain regions called hypothalamus and thalamus, which have been associated with EEG (electroencephalogram) rhythms during sleep. The activation of this circuit signals the termination of light sleep: using a recent technology called optogenetics, the researchers made neurons from the hypothalamus controllable with millisecond-timescale light pulses and showed that their transient activation during light sleep induced rapid awakenings, while their chronic activation maintains prolonged wakefulness. In contrast, optogenetic silencing of this circuit stabilizes light sleep and increases its intensity. In a translational analogy, hyperactivity of this circuit may cause insomnia, while its hypo-activity could be responsible for hypersomnia, making it a new therapeutical target for sleep disorders.
Causing emergence from anesthesia and unconsciousness
Interestingly, the arousal power of this circuit is so strong that its activation precipitates emergence from anesthesia and the recovery of consciousness. «This is exciting discovery since therapeutical approaches to recover from a vegetative or minimally conscious state are quite limited», says Adamantidis. Non-selective deep brain electrical stimulation has been used with some success, however the underlying brain mechanisms remain unclear. In this study, Adamantidis, Gutierrez Herrera and collaborators nailed down a selective brain circuit important for the recovery of consciousness.
The dual findings of the Bernese researchers shine light on the brain mechanism of arousal and opens new door for tailored medical treatment of sleep perturbances, and provide a roadmap for arousing patients from a vegetative or minimally conscious state. However, Adamantidis emphasizes that «even though we made an important step forward now, it will take some time before novel therapeutical strategies will be designed based on our results».

Drug that boosts activity in the brain's 'garbage disposal' system may slow Alzheimer's disease

Dec. 22, 2015

A drug that boosts activity in the brain's "garbage disposal" system can decrease levels of toxic proteins associated with Alzheimer's disease and other neurodegenerative disorders and improve cognition in mice, a new study by neuroscientists at Columbia University Medical Center (CUMC) has found. The study was published today in the online edition of Nature Medicine.
"We have shown for the first time that it's possible to use a drug to activate this disposal system in neurons and effectively slow down disease," said study leader Karen E. Duff, PhD, professor of pathology and cell biology (in psychiatry and in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain) at CUMC and at the New York State Psychiatric Institute. "This has the potential to open up new avenues of treatment for Alzheimer's and many other neurodegenerative diseases." The drug used was rolipram, which causes nausea and thus is not a good drug for use in humans, but similar drugs do not incur nausea as a side effect and could go into clinical trials very quickly,
To remain healthy, brain cells must continually clear out old, worn, or damaged proteins, a task performed by a small molecular cylinder called the proteasome. The proteasome acts as a kind of garbage disposal, grinding up the old proteins so they can be recycled into new ones. In neurodegenerative diseases, proteins tagged for destruction accumulate in the brain's neurons, suggesting that the cell's proteasomes are impaired.
Using a mouse model of neurodegeneration, the researchers first discovered that tau--a toxic protein that accumulates in Alzheimer's and other brain degenerative diseases--sticks to the proteasome and slows down the protein disposal process.
Administering rolipram activated the proteasome and restored protein disposal to normal levels. The drug also improved the memory of diseased mice to levels seen in healthy mice.
Rolipram has been tested before in mice and was shown to improve memory, but the mechanism for how this occurred was unclear. The new research shows that by inhibiting of the PDE-4 enzyme, rolipram produces a physical change in the proteasome that increases its activity.
"We still don't know exactly where the activation is happening, but what's new is that we can modify the proteasome to increase its activity. There could be many other ways to do this," said the study's first author, Natura Myeku, PhD, an associate research scientist in pathology and cell biology at CUMC.
Drugs that target proteasomes in this way should work for any disease caused by the accumulation of abnormal proteins, including Alzheimer's, Huntington's, Parkinson's and frontotemperoral dementia.
"Treatments that speed up these cell disposal mechanisms should, in theory, only degrade abnormal proteins. We don't need to know what the toxic form of the protein is," Dr Duff said. "In Alzheimer's disease, there are at least four different types: amyloid, tau, alpha-synuclein, and TDP43. A well-functioning proteasome can clear out everything at once."
"This exciting research from Dr. Duff's team advances our basic understanding of the proteasome system, provides a way to repair the system when it breaks, and alleviates symptoms of neurodegenerative disorders," said Rod Corriveau, PhD, program director at the National Institute of Health's National Institute of Neurological Disorders and Stroke, which provided funding for the study.
Columbia University Medical Center

Benjamin Wolozin receives $500,000 award in Alzheimer's Disease Drug Discovery Research

Published on December 22, 2015 

Research that leads to improved therapies for Alzheimer's disease (AD) patients is one goal of Boston University School of Medicine professor of pharmacology and neurology Benjamin Wolozin, MD, PhD. He was one of six researchers awarded a two-year, $500,000 award in Alzheimer's Disease Drug Discovery Research by the Edward N. & Della L. Thome Memorial Foundation.

Wolozin has been studying the pathophysiology of AD, amyotrophic lateral sclerosis and Parkinson's disease (PD) for nearly 20 years and has made numerous contributions to the current field of understanding of neurodegenerative diseases. He has published more than 150 papers and book chapters on the topic in such high impact journals as Science, Nature and PNAS. He also holds four patents in the AD and PD fields and is the co-founder of the biotechnology company Aquinnah Pharmaceuticals, Inc.

The Edward N. & Della L. Thome Memorial Foundation was created in 2002 with the mission of advancing the health of older adults through support of direct service projects and medical research on disease and disorders affecting them. Each year they award $500,000 to a faculty member at a non-profit academic, medical, non-governmental or research institution in the United States with the purpose of furthering this objective.

The Edward N. & Della L. Thome Memorial Foundation, Bank of America, N.A., Trustee, Awards Program in Alzheimer's Disease Drug Discovery Research is administered by The Medical Foundation, a division of Health Resources in Action (HRiA). HRiA is a nonprofit organization in Boston that advances public health and medical research.
Boston University Medical Center

Novel drug candidate prevents nerve cell damage in mouse model of Parkinson's disease

Published on December 18, 2015
A team of scientists at the University of Nebraska Medical Center (UNMC) and Longevity Biotech, Inc., has demonstrated that neuroprotection could be attained in preclinical models by a novel drug candidate that changes immune responses.
The results, published today in the Journal of Neuroscience, describe the prevention of nerve cell damage in a mouse model of Parkinson's disease. Notably, the drug protected nerve cells that produce dopamine, which is the chemical responsible for agility and movement that is lost in human disease.
"The results are exciting as they provide a bridge between the immune system and nerve cell protection in Parkinson's disease," said Scott Shandler, Ph.D., co-founder and CEO of Longevity Biotech.
"The idea was birthed nearly a decade ago when specific types of circulating blood cells called lymphocytes were found to damage the types of nerve cells responsible for disease," said Howard Gendelman, M.D., the Margaret R. Larson Professor and chair of the UNMC Department of Pharmacology and Experimental Neuroscience. "The new Longevity Biotech drug (LBT-3627) was able to change the function of these cells from killing the nerve cells to protecting them. This is especially significant for the Nebraska team, as the mechanism parallels closely the human trials nearing completion for Parkinson's patients."
LBT-3627 is similar to the naturally occurring vasoactive intestinal peptide (VIP), a well-established anti-inflammatory peptide with beneficial effects across a variety of disorders. VIP is rapidly degraded by the body and is unable to distinguish between its two naturally intended receptors (VPAC1 vs. VPAC2). These limitations have stymied prior translational success using VIP.
In contrast, LBT-3627 specifically targets VPAC2 and demonstrates impressive biological durability. In addition, LBT-3627 has the potential to be administered orally, Dr. Shandler said, which would further improve its clinical prospects and make it more accessible for people with Parkinson's disease.
Preclinical studies performed by the UNMC team demonstrated that LBT-3627 could achieve up to 80 percent protection of dopamine-producing nerve cells in a mouse model of Parkinson's disease. Furthermore, the immune transformation also affected primary scavenger cells called microglia cells that were found ultimately responsible for the neuroprotective activities observed that halted brain damage.
"The key finding in our study was that a specific white blood cell subset was produced as a consequence of LBT-3627 treatment and provided protection of dopamine producing nerve cells from being damaged," Dr. Gendelman said. "The neurotoxic immune reaction was halted and LBT-3627 was able to prevent disease."
"There are limited therapeutic strategies available to Parkinson's patients," said Marco Baptista, Ph.D., senior associate director of research programs at The Michael J. Fox Foundation for Parkinson's Research, which supported this work together with the National Institute of Neurological Disorders and Stroke and a generous gift from the Blumkin Foundation in Nebraska. "This approach shows one avenue to potentially protect the brain cells affected by Parkinson's disease and alter disease progression."
Dr. Shandler said Longevity Biotech is currently progressing LBT-3627 through preclinical development and hopes to begin a Phase I clinical trial in humans by 2017.


Dec. 23, 2015
Melanoma incidence is higher in people affected by Parkinson's Disease but the genetic link shared by both diseases was unknown. The Parkin gene (PARK2) is often mutated in Parkinson's Disease and is consequently sometimes a genetic cause of Parkinson's Disease. However, PARK2 is also a tumor suppressor gene both of melanoma predisposition and progression. Melanoma is a form of skin cancer more common in Parkinson's Disease. For more information go to :
An in-depth analysis of the PARK2 (Parkin) gene showed that mutations were present far more often in Parkinson's Disease, making Parkinson's Disease nearly four times more likely. The formation of the Parkin gene occurs in melanocytes but not in most cells in which there is melanoma. The formation of the Parkin gene in melanoma cell lines resulted in a drastic reduction of cell proliferation. Inhibition of the Parkin gene in melanocytes stimulated their proliferation.
The results show an important role for the Parkin gene (PARK2), not only in Parkinson's Disease, but also as a tumor suppressor both in melanoma predisposition and progression, which could explain the association between Parkinson's Disease and melanoma.

Reference : Journal of the National Cancer Institute [2015] 108 (3) pii : djv340 (H.H.Hu, C.Kannengiesser, S.Lesage, J.André, S.Mourah, L.Michel, V.Descamps, N.Basset-Seguin, M.Bagot, A.Bensussan, C.Lebbé, L.Deschamps, P.Saiag, M.T.Leccia, B.Bressac-de- Paillerets, A.Tsalamlal, R.Kumar, S.Klebe, B.Grandchamp, N.Andrieu-Abadie, L.Thomas, A.Brice, N.Dumaz, N.Soufir)
Complete abstract :

©2015 Viartis

Tuesday, December 22, 2015



Drinking beer could prevent the damage of the brain cells, says a research carried out by Jianguo Fang and his colleagues of Lanzhou University’s school of chemistry. Drinking liquor is not a much appreciated practice in the past but partying has become a part of life these days. While the goodness of the wine is well known, it’s time to know something more about beer.
Beer is not usually considered an evil for health when taken in reasonable quantity, but the goodness of beer is sure to amaze the beer lovers. A compound called xanthohumol present in the beer is observed to have anti-carcinogenic, anti-oxidation and cardiovascular-protection properties.
During brewing, an ingredient called hops is added to the beer that gives a bitter and tangy taste to it. Hops are the female flower of the hops plant known to have quite some medicinal values. Hops are the source of the compound xanthohumol present in the beer that renders goodness to the beer. These xanthohumol are observed to protect neuronal cells present in the brain and thereby slows down the development of brain disorders, reports Fangs and his team.
The oxidative damage to the neuronal cells is responsible for the development of brain diseases, according to the research, said Fang. Brain defects like Alzheimer’s disease, Parkinson’s disease and other neurodegenerative conditions could be prevented or slowed down by the preventing the oxidative damage to these neuronal cells.
Alzheimer’s disease is a type of dementia that causes interruption in memory, thinking and behaviour in a person’s regular life, whereas Parkinson’s disease is a chronic and progressive movement disorder due to the death of vital nerve cells or neurons. No cure has been found for these neurodegenerative diseases so far, and if this research is to be believed, then it is no wonder a joy to the beer brewers and beer lovers.
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