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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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Monday, November 20, 2017

Benzodiazepines Increase Mortality in Persons with Alzheimer’s Disease

NEUROSCIENCE NEWS   NOVEMBER 20, 2017
Source: University of Eastern Finland.

Summary: Researchers report an elevated risk of death in Alzheimer’s patients who use benzodiazapines.

Although several treatment guidelines state that non-pharmacological options are the first-line treatment of anxiety, agitation and insomnia in persons with dementia, benzodiazepines and related drugs are frequently used in the treatment of these symptoms. NeuroscienceNews.com image is in the public domain.


Benzodiazepine and related drug use is associated with a 40 per cent increase in mortality among persons with Alzheimer’s disease, according to a new study from the University of Eastern Finland. The findings were published in the International Journal of Geriatric Psychiatry.

The study found that the risk of death was increased right from the initiation of benzodiazepine and related drug use. The increased risk of death may result from the adverse events of these drugs, including fall-related injuries, such as hip fractures, as well as pneumonia and stroke.

The study was based on the register-based MEDALZ (Medication Use and Alzheimer’s Disease) cohort, which includes all persons diagnosed with Alzheimer’s disease in Finland during 2005-2011. Persons who had used benzodiazepines and related drugs previously were excluded from this study, and therefore, the study population consisted of 10,380 new users of these drugs. They were compared with 20,760 persons who did not use these drugs.

Although several treatment guidelines state that non-pharmacological options are the first-line treatment of anxiety, agitation and insomnia in persons with dementia, benzodiazepines and related drugs are frequently used in the treatment of these symptoms. 

If benzodiazepine and related drug use is necessary, these drugs are recommended for short-term use only. These new results encourage more consideration for benzodiazepine and related drug use in persons with dementia.


ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Source: Laura Saarelainen – University of Eastern Finland
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Singer et al., JNeurosci (2017).
Original Research: Abstract for “Risk of death associated with new benzodiazepine use among persons with Alzheimer disease: A matched cohort study” by Laura Saarelainen, Anna-Maija Tolppanen, Marjaana Koponen, Antti Tanskanen, Jari Tiihonen, Sirpa Hartikainen, and Heidi Taipale in International Journal of Geriatric Psychiatry. Published online November 15 2017 doi:10.1002/gps.4821


Abstract

Risk of death associated with new benzodiazepine use among persons with Alzheimer disease: A matched cohort study
Objective

To investigate the risk of death associated with new benzodiazepine and related drug (BZDR) use in a nationwide cohort of persons with Alzheimer disease (AD).

Methods
The register-based MEDALZ cohort, including all community-dwelling Finns diagnosed with AD during 2005 to 2011 (n = 70 718), was used. Clinically verified AD diagnoses were obtained from the Special Reimbursement Register. Drug use periods were modeled from BZDR purchases, derived from the Prescription Register. To study new users, persons who had any BZDR use during the year preceding the AD diagnosis were excluded.
For each person initiating BZDR use (n = 10 380), 2 nonusers (n = 20 760) were matched on age, gender, and time since AD diagnosis. The outcome was 180-day mortality, and BZDR use was compared with nonuse with Cox regression. Multivariable analyses were adjusted for Charlson comorbidity index, socioeconomic position, hip fractures, psychiatric disorders, substance abuse, stroke, and other psychotropic drug use.

Results

During the follow-up, 5 excess deaths per 100 person-years occurred during BZDR use in comparison to nonuse, and mortality rates were 13.4 (95% confidence interval [CI], 12.2-14.5) and 8.5 (95% CI, 7.9-9.1), respectively. Benzodiazepine and related drug use was associated with an increased risk of death (adjusted hazard ratio = 1.4 [95% CI, 1.2-1.6]), and the association was significant from the initiation of use. Benzodiazepine use was associated with an increased risk of death, whereas benzodiazepine-related drug use was not.

Conclusions

Benzodiazepine and related drug use was associated with an increased risk of death in persons with AD. Our results support treatment guidelines stating that nonpharmacological approaches should be the first-line option for symptomatic treatment of AD.
“Risk of death associated with new benzodiazepine use among persons with Alzheimer disease: A matched cohort study” by Laura Saarelainen, Anna-Maija Tolppanen, Marjaana Koponen, Antti Tanskanen, Jari Tiihonen, Sirpa Hartikainen, and Heidi Taipale in International Journal of Geriatric Psychiatry. Published online November 15 2017 doi:10.1002/gps.4821

http://neurosciencenews.com/benzidoazepine-alzheimers-7990/

New push on Parkinson’s disease

BY DAVID JENSEN POSTED 11.20.2017





A “new era” in the search for a cure for Parkinson’s disease was heralded this month in an article in a prominent scientific journal that explored research involving more than $52 million and an organization called GForce-PD. 
The news was accompanied by a cry for more support for Parkinson’s research from the $3 billion California stem cell agency, which has pumped $49 million in Parkinson’s studies over the last 13 years.
Parkinson’s is a devastating disease that afflicts 10 million people in the world and 125,000 in California.
Jeanne Loring, director of the Scripps Center for Regenerative Medicine in La Jolla, and also a participant in the GForce initiative, said this week that CIRM has not supported Parkinson’s research at the level of the other enterprises involved in GForce. 
In an item she wrote for The Niche, a blog published by UC Davis researcher Paul Knoepfler, she listed $52.3 million in support plus substantial backing from BlueRock Therapeutics, which is financed with $225 million from Bayer AG and Versant Ventures. BlueRock, a Cambridge, Mass., firm, says on its web site, “Our most advanced therapeutic candidate, for Parkinson’s disease, will enter the clinic in 2018.
Parkinson’s is a devastating disease that afflicts 10 million people in the world and 125,000 in California. One of those persons, David Higgins of San Diego, currently serves on the board of the stem cell agency, formally known as the California Institute for Regenerative Medicine (CIRM). Another, Joan Samuelson, was one of the original board members in 2004 and a fervent but often frustrated voice for Parkinson’s research at many CIRM board meetings.

“We hope that CIRM will follow the example of New York, the EU, and Japan, and invest more in our project to provide neuron replacement therapy for Californians with Parkinson’s disease.” — Jeanne Loring
Actor Michael J. Fox, who made TV ads for the 2004 ballot initiative that created the stem cell agency, is also among the those living with the disease. Others with the affliction included the late boxing champion Muhammad Ali and famed semiconductor pioneer Andy Grove
Loring wrote on The Niche about a meeting in Japan earlier this year dealing with the research teams in the GForce project.
“The Kyoto meeting was unprecedented in my experience,” she said.  “Instead of competing, the four groups cooperated and shared plans for their proposed clinical trials.  We agreed to harmonize our trials and stay in communication about our progress.  All of us plan to start clinical trials within two years.”
“Since my team has been recognized by the international GForce initiative devoted to safe effective therapy for PD, we hope that CIRM will follow the example of New York, the EU, and Japan, and invest more in our project to provide neuron replacement therapy for Californians with Parkinson’s disease,” Loring continued.
“While we hope to gain more support from CIRM, we are determined to follow through with our clinical trial, with or without CIRM.  It will just be more difficult without their help. The patients and their advocates inspire us, and we won’t let them down,” she said.
Loring added more information on Sunday (Nov. 19) concerning CIRM funding. She told the California Stem Cell Report.
|”We started our pre-clinical PD studies in 2011, with funding from Summit for Stem Cell. The first and only funding we received from CIRM for PD research was in 2016.
“Before 2011, CIRM invested $41,838,336. Since 2011, CIRM has invested $7,357,468. This means that the majority of the funding went to projects that didn’t lead to any translational or clinical applications.
“There are currently three active grants working on Parkinson’s disease, for a total of $4.9 million. We have the only translational grant, and it will expire in March 2018. All but $650,000 runs out by the spring of 2018.
“There are no more grants forthcoming for our work. The Scaled Biolabs grant awarded this year is a partnership with us. Birgitt Schuele’s grant is basic research, not a cell therapy.
(Below are the three active grants identified by Loring.)
2017

Ed’s Note: David Jensen is a retired newsman who has followed the affairs of the $3 billion California stem cell agency since 2005 via his blog, the California Stem Cell Report, where this story first appeared. He has published more than 4,000 items on California stem cell matters in the past 11 years.

http://capitolweekly.net/n-ew-push-parkinsons-disease-stem-cell/

Vibrating sensors could identify blood biomarkers, improve early-stage detection, treatment of numerous diseases

November 20, 2017

A piezoelectrically actuated pipette system is used as an inexpensive means to detect biological molecules associated with specific diseases, infection or other medical conditions. Purdue University researchers believe the test could be the early detection of traumatic brain injury in athletes, particularly high school football and soccer players.


WEST LAFAYETTE, Ind. – Purdue Universityresearchers have found a method of identifying biological markers in small amounts of blood that they believe could be used to detect a myriad of diseases, infections and different medical conditions at early stages.
Jeffrey Rhoads, a professor in Purdue’s School of Mechanical Engineering; George Chiu, a professor in Purdue’s School of Mechanical Engineering, School of Electrical and Computer Engineering, and Department of Psychological Sciences; and Eric Nauman, a professor in the School of Mechanical Engineering, Department of Basic Medical Sciences and the Weldon School of Biomedical Engineering, are part of a team of researchers that has created microelectromechanical resonators, or small vibrating sensors, that can detect these biomarkers using just a drop or two of blood. The plate-style resonant sensors allows sensitive, inexpensive detection of biomarkers that can signify disease, illness or trauma.
“The goal here is to find the disease so early that you can treat it without invasive surgery,” Rhoads said. “The test looks for a particular protein related to a disease, so you could use this for the detection of many different diseases.”
The sensors use a piezoelectrically actuated resonant microsystem, which when driven by electricity can sense a change in mass. The sensitivity of the resonator increases as the resonant frequency increases, making high-frequency resonators excellent candidates for biomarker detection, Rhoads said. The method also is much faster and less expensive than other types of medical tests.
The paper was published in IEEE Sensors Letters (http://ieeexplore.ieee.org/document/8093625).
Rhoads said they discovered a way to conduct the test that identifies a minute amount of protein in a very small amount of blood.
“Detecting biomarkers is like trying to find a handful of needles in a large haystack. So we devised a method that divided the large haystack into smaller haystacks,” Rhoads said. “Instead of having a single sensor, it makes more sense to have an array of sensors and do statistical-based detection.”
One of the first uses for the test could be the early detection of traumatic brain injury in athletes, particularly high school football and soccer players. A Purdue research team, known as the Purdue Neurotrauma Group, began studying the effects of head injuries in 2009 and found that concussions are usually caused by multiple hits over time and not by a single blow, as commonly believed. The group, which includes Nauman and Thomas Talavage, a professor in the schools of Electrical and Computer Engineering and Biomedical Engineering, has studied football and women’s soccer at the high school and collegiate levels.
Research into the effects of repeated head impacts on high school football players has shown changes in brain chemistry and metabolism even in players who have not been diagnosed with concussions, Nauman said.
Concussions now are diagnosed using a battery of tests, often starting with asking an athlete whether he knows what time it is or where he is. They then move to cognitive tests that grade concussion symptoms along a scale. Nauman said that while 5 percent to 10 percent of high school football players will be diagnosed with concussions, more than 50 percent of those athletes will experience neurological changes before a concussion is diagnosed. Researchers have learned that a concussion is generally an accumulation of injury and the test they have developed can detect the traumatic brain injury before it becomes symptomatic.
“You do enough damage, you knock out enough systems and eventually you have symptoms,” Nauman said.
The test the Purdue researchers developed can detect minute amounts of proteins, including protein from glial cells, which surround neurons in the brain. The proteins are secreted in relatively high concentrations in cerebrospinal fluid of victims of traumatic brain injury. Prior studies have found that a small amount of fluid leaked through the blood-brain barrier and got into the bloodstream of victims.
“Essentially the idea is that if you can measure anything that passes through the blood-brain barrier from the brain into the blood, it's a problem because it should stay in the brain,” Nauman said.
The test also is inexpensive so a high school football team could do several mass screenings a season, Rhoads said. Nauman said the Purdue Neurotrauma Group hopes to test high school athletes next fall.
The test also could be used for the early detection of Alzheimer’s disease and Parkinson’s disease, Nauman said. “You can basically look for general neurodegeneration, not just in athletes.”
The researchers believe the test also could be used to detect countless other diseases. They are looking for licensees to use the test to search for other small amounts of protein that are early signs of disease.
“There’s a whole host of diseases and different conditions where, if you could find these things in small quantities early on and just make it part of a standard workup, you could decrease health-care costs greatly,” Nauman said.
The researchers have filed a patent application through the Purdue Research Foundation’s Office of Technology Commercialization.
About Purdue Office of Technology Commercialization
The Purdue Office of Technology Commercialization operates one of the most comprehensive technology transfer programs among leading research universities in the U.S. Services provided by this office support the economic development initiatives of Purdue University and benefit the university's academic activities. The office is managed by the Purdue Research Foundation, which received the 2016 Innovation and Economic Prosperity Universities Award for Innovation from the Association of Public and Land-grant Universities. For more information about funding and investment opportunities in startups based on a Purdue innovation, contact the Purdue Foundry at foundry@prf.org. For more information on licensing a Purdue innovation, contact the Office of Technology Commercialization at innovation@prf.org.
Purdue Research Foundation contact: Tom Coyne, 765-588-1044, tjcoyne@prf.org 

Sources: Jeffrey Rhoads, 765-494-5630, jfrhoads@purdue.edu

Eric Nauman, enauman@purdue.edu
Abstract:
Microelectromechanical resonators enable the sensitive and inexpensive detection of biological molecules associated with specific diseases, infections, or other medical conditions that are commonly referred to as biomarkers. The focus of this effort is the detection of s100β, a protein biomarker that is secreted in relatively high concentrations in the cerebrospinal fluid of victims of Traumatic Brain Injury (TBI). Sensor functionalization via polymer/antibody coatings is explored as a method to allow for the adsorption of s100β onto the surface of the resonator. A high-precision, piezoelectrically actuated pipette system is utilized to improve sensor functionalization and biomarker exposure techniques. High-frequency resonators are utilized for their high mass sensitivity. Frequency domain characterization of multiple sensors reveals shifts in their resonant peaks caused by the adsorption of s100β. Successful detection of s100β was achieved (p=0.000012) at sensitivities that are theoretically sufficient to enable the diagnosis of TBI.
Published in: IEEE Sensors Letters ( Volume: PP, Issue: 99 )

http://www.purdue.edu/newsroom/releases/2017/Q4/vibrating-sensors-could-identify-blood-biomarkers,-improve-early-stage-detection,-treatment-of-numerous-diseases.html

First patient implanted with novel drug delivery system from Renishaw for Parkinson’s

November 20, 2017

First patient has been implanted with a novel drug delivery system, developed by Renishaw, for a new clinical study investigating it as a delivery method for cerebral dopamine neurotrophic factor (CDNF) as a treatment for Parkinson’s disease.



The procedure was performed at Karolinska University Hospital in Stockholm, Sweden, and represents the beginning of a joint clinical study between Renishaw and Herantis Pharma.
“Renishaw’s drug delivery system could be revolutionary in improving treatment options for Parkinson’s disease,” explained Paul Skinner, general manager for Renishaw's Neurological Products Division. “The system enables the delivery of large drug molecules, such as CDNF, directly into the brain — circumventing the blood brain barrier.
“The drug delivery system consists of four catheters which, during the procedure, are accurately implanted into the patient’s putamen, one of the key regions of the brain affected by Parkinson’s disease,” he continued. “The catheters converge in a port mounted to the skull behind the ear, through which drugs will be administered on a monthly basis as part of the study. The system can also be used with other new drug candidates that need to be delivered to precise areas of the brain, which could be crucial in the development of treatments for this and other debilitating diseases.”
This clinical study, which has received funding from Horizon 2020, will involve18 volunteers across three sites — two in Sweden and one in Finland. It will evaluate the safety and tolerability of the drug delivery system and CDNF, a large molecule that could slow the progression of Parkinson’s disease, improving the quality of life for patients and prolong their lives.
Following this study, it is hoped that Renishaw’s delivery system will be used in clinical trials for other neurological disorders.
https://www.epmmagazine.com/technology/first-patient-implanted-with-novel-drug-delivery-system-from/

Researchers Describe a New Biology of Alzheimer’s Disease

NEUROSCIENCE NEWS   NOVEMBER 20, 2017
Source: Boston University School of Medicine.


Summary: Researchers present a new model for the biology of Alzheimer’s disease in a Nature Neuroscience study. They note the findings could help lead to a new approach to treating the neurodegenerative disease.


In the current study, the researchers use this new model and show that reducing the level of stress granule proteins yields strong protection, possibly by reducing persistent pathological stress granules as well as changing the type of tau clumping that occurs. NeuroscienceNews.com image is in the public domain.



In a new study, researchers from Boston University School of Medicine (BUSM) describe a unique model for the biology of Alzheimer’s disease (AD) which may lead to an entirely novel approach for treating the disease. The findings appear in the journal Nature Neuroscience.

AD is a major cause of disease in the elderly and places a huge financial cost on the health care system. Scientists have known for a long time that two proteins (beta-amyloid and tau) clump and accumulate in the brains of Alzheimer patients, and this accumulation is thought to cause nerve cell injury that results in dementia.

Recent work by these BUSM researchers has shown that the clumping and accumulation of tau occurs as a normal response to stress, producing RNA/protein complexes termed “stress granules,” which reflect the need for the brain to produce protective proteins. The persistence of this “stress response” leads to excessive stress, the accumulation of pathological stress granules, and the accumulation of clumped tau, which drives nerve cell injury and produces dementia.

In the current study, the researchers use this new model and show that reducing the level of stress granule proteins yields strong protection, possibly by reducing persistent pathological stress granules as well as changing the type of tau clumping that occurs.

The team hypothesized that they could delay the disease process by reducing stress granules and decreasing this persistent stress response by genetically decreasing TIA1, which is a protein that is required for stress granule formation. Reducing TIA1 improved nerve cell health and produced striking improvements in memory and life expectancy in an experimental model of AD.

Although the experimental models had better memory and longer lives, the team observed more clumped tau in the form of neurofibrillary tangles. To explain how this might be associated with a better outcome, the researchers looked at the type of tau pathology and showed that reducing TIA1 dramatically lowered the amount of tiny clumps, which are termed tau oligomers and are particularly toxic. “Reducing TIA1 shifted tau accumulation from small to large clumps, decreasing the amount of small tau clumps and producing a proportional increase in the large tau clumps that generate neurofibrillary tangles and are less toxic,” said corresponding author Benjamin Wolozin, MD, PhD, professor of pharmacology & experimental therapeutics at BUSM.

“This ability of TIA1 reduction to provide protection opens up a new chapter in our understanding of the biology of Alzheimer’s disease and also suggests new avenues for pharmacotherapy for this disease and other tauopathies,” said Wolozin.
ABOUT THIS NEUROSCIENCE RESEARCH ARTIcle
Funding: Funding for this study was provided by the National Institutes of Health (AG050471, NS089544, ES020395, R01 AG054199), BrightFocus Foundation; the Alzheimer Association; Cure Alzheimer’s Fund and the Thome Medical Foundation; the UGC-Raman Fellowship; The Government of India and the Paul F. Glenn Foundation.
Benjamin Wolozin is Co-Founder and Chief Scientific Officer for Aquinnah Pharmaceuticals Inc.
Source: Gina DiGravio – Boston University School of Medicine
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Abstract for “Reducing the RNA binding protein TIA1 protects against tau-mediated neurodegeneration in vivo” by Daniel J. Apicco, Peter E. A. Ash, Brandon Maziuk, Chelsey LeBlang, Maria Medalla, Ali Al Abdullatif, Antonio Ferragud, Emily Botelho, Heather I. Ballance, Uma Dhawan, Samantha Boudeau, Anna Lourdes Cruz, Daniel Kashy, Aria Wong, Lisa R. Goldberg, Neema Yazdani, Cheng Zhang, Choong Y. Ung, Yorghos Tripodis, Nicholas M. Kanaan, Tsuneya Ikezu, Pietro Cottone, John Leszyk, Hu Li, Jennifer Luebke, Camron D. Bryant & Benjamin Wolozin in Nature Neuroscience. Published online November 20 2017 doi:10.1038/s41593-017-0022-z


Abstract

Reducing the RNA binding protein TIA1 protects against tau-mediated neurodegeneration in vivo

Emerging studies suggest a role for tau in regulating the biology of RNA binding proteins (RBPs). We now show that reducing the RBP T-cell intracellular antigen 1 (TIA1) in vivo protects against neurodegeneration and prolongs survival in transgenic P301S Tau mice. Biochemical fractionation shows co-enrichment and co-localization of tau oligomers and RBPs in transgenic P301S Tau mice. Reducing TIA1 decreased the number and size of granules co-localizing with stress granule markers. Decreasing TIA1 also inhibited the accumulation of tau oligomers at the expense of increasing neurofibrillary tangles. Despite the increase in neurofibrillary tangles, TIA1 reduction increased neuronal survival and rescued behavioral deficits and lifespan. These data provide in vivo evidence that TIA1 plays a key role in mediating toxicity and further suggest that RBPs direct the pathway of tau aggregation and the resulting neurodegeneration. We propose a model in which dysfunction of the translational stress response leads to tau-mediated pathology.

“Reducing the RNA binding protein TIA1 protects against tau-mediated neurodegeneration in vivo” by Daniel J. Apicco, Peter E. A. Ash, Brandon Maziuk, Chelsey LeBlang, Maria Medalla, Ali Al Abdullatif, Antonio Ferragud, Emily Botelho, Heather I. Ballance, Uma Dhawan, Samantha Boudeau, Anna Lourdes Cruz, Daniel Kashy, Aria Wong, Lisa R. Goldberg, Neema Yazdani, Cheng Zhang, Choong Y. Ung, Yorghos Tripodis, Nicholas M. Kanaan, Tsuneya Ikezu, Pietro Cottone, John Leszyk, Hu Li, Jennifer Luebke, Camron D. Bryant & Benjamin Wolozin in Nature Neuroscience. Published online November 20 2017 doi:10.1038/s41593-017-0022-z

http://neurosciencenews.com/alzheiemrs-neurobiology-7986/

MRI Uncovers Brain Abnormalities in People With Anxiety and Depression

NEUROSCIENCE NEWS   NOVEMBER 20, 2017
Source: RSNA.


Summary: Researchers discover common and specific changes to the brain’s gray matter in patients with major depressive disorder and social anxiety disorder.

There are significant cortical thickness differences among the three groups. All regions survived clusterwise-correction. NeuroscienceNews.com image is credited to Radiological Society of North America.


Researchers using MRI have discovered a common pattern of structural abnormalities in the brains of people with depression and social anxiety, according to a study presented being next week at the annual meeting of the Radiological Society of North America (RSNA).

Major depressive disorder (MDD), often simply referred to as depression, is a serious condition. The condition can have a debilitating effect on an individual’s life. People with MDD often lose interest in activities they once enjoyed and sometimes find it difficult just to get out of bed. At times, they may feel suicidal. About 16 million Americans have MDD.

Social anxiety disorder, or SAD, is an intense fear of being watched and judged by others. Symptoms can be extreme enough to interfere with daily activities. People with this disorder have difficulty developing and maintaining social and romantic relationships. About 15 million American adults have social anxiety disorder.

Both conditions share some clinical symptoms, suggesting the two disorders may have similar brain mechanisms. However, few studies have directly compared the brain structural effects of the two disorders, said the author of the new study, Youjin Zhao M.D., Ph.D., from Sichuan University in Chengdu, China.

Dr. Zhao and co-author Su Lui, M.D., used MRI to assess alterations in the brain’s gray matter among MDD and SAD patients. They focused on the thickness of the cortex, which is the outer layer of the cerebrum, or principal part of the brain.

The researchers acquired and analyzed high-resolution images from 37 MDD patients, 24 SAD patients and 41 healthy control individuals. Both MDD and SAD patients, relative to healthy controls, showed gray matter abnormalities in the brain’s salience and dorsal attention networks. The salience network is a collection of brain regions that determine which stimuli are deserving of our attention, while the dorsal attention network plays an important role in focus and attentiveness.

“Our findings provide preliminary evidence of common and specific gray matter changes in MDD and SAD patients,” Dr. Zhao said. “Future studies with larger sample sizes combined with machine learning analysis may further aid the diagnostic and prognostic value of structural MRI.”

The differences between the MDD and SAD patients and the healthy controls related to either thickening or thinning of the cortex. For instance, both MDD and SAD patients, relative to healthy controls, showed cortical thickening in the insular cortex, a brain region vital to perception and self-awareness.

It is still unclear exactly what the relationship is between the clinical manifestations of MDD and SAD and cortical thickening in brain regions like the anterior cingulate cortex, a part of the brain associated with emotion, Dr. Zhao said.

“First, it is possible that a greater cortical thickness may reflect a compensatory mechanism that is related to inflammation or other aspects of the pathophysiology,” she said. “Second, greater anterior cingulate cortical thickness could be the result of both the continuous coping efforts and emotion regulation attempts of MDD and SAD patients.”

As for cortical thinning, Dr. Zhao said that other research provides convincing evidence to support the theory that reduced cortical layer thickness in some brain regions may result in the decreased thickness of the frontal lobe, a large part of the brain that is involved in variety of functions, including emotion.

The researchers also found disorder-specific involvement of the brain’s “fear circuitry” in patients with SAD and involvement of the visual recognition network in patients with MDD. Alterations in the brain within the region of the visual recognition network might be related to impaired selective attention and working memory in MDD, Dr. Zhao indicated.

“The visual recognition network is involved in emotional facial processing, which is crucial for social functioning,” she said. “Depression has been associated with structural alterations in these regions.”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Source: Linda Brooks – RSNA
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Radiological Society of North America.
Original Research: The study will be presented at RSNA 2017 103rd Scientific Assembly and Annual Meeting.

RSNA “MRI Uncovers Brain Abnormalities in People With Anxiety and Depression.” NeuroscienceNews. NeuroscienceNews, 20 November 2017.
<http://neurosciencenews.com/depression-anxiety-mri-7987/>.

http://neurosciencenews.com/depression-anxiety-mri-7987/

Additional Blood Cell Monitoring Added to Tozadenant Trials Following Adverse Events

NOVEMBER 20, 2017   BY PATRICIA INACIO, PHD



Acorda Therapeutics announced that it will now monitor blood cell counts on a weekly basis in Parkinson’s disease patients enrolled in the company’s Phase 3 program investigating the safety and effectiveness of tozadenant.
The update to the clinical trial responds to cases of patients developing agranulocytosis, a severe drop in white blood cells that are vital to fighting infections. The cases are believed to be linked to tozadenant therapy, and in some instances, they were associated with sepsis and death.
“We have taken these steps in the best interests of the safety of patients in the tozadenant studies, which is our top priority,” Ron Cohen, MD, Acorda’s president and chief executive officer, said in a press release.
Acorda has put on hold new enrollment in the long-term safety studies while awaiting discussions with the independent Data Safety Monitoring Board (DSMB) and the U.S. Food and Drug Administration (FDA).
“Contingent on further input from the DSMB and FDA, we continue to expect to report efficacy and safety results of the double-blind Phase 3 study in the first quarter of 2018,” he added.
Until now, approximately 890 patients have received tozadenant in the clinical trials, and 234 patients were in a placebo group. Treatment with tozadenant has been linked to seven cases of sepsis, five of which were fatal. Four of the patients developed agranulocytosis.
Acorda launched two Phase 3 trials early this year. TOZ-CL-06 (NCT03051607), an international, multicenter, open-label study performed over 12 months, is investigating the long-term safety of tozadenant as adjunctive therapy in levodopa-treated patients experiencing end-of-dose “wearing-off.” In the trial, patients are first receiving tozadenant at a dose of 120 mg twice a day. Following week 2, researchers may adjust the dose and reduce it to 60 mg or continue with the 120 mg dose. The results are due in early 2018.
In the TOZ-CL-05 trial (NCT02453386), patients are randomly assigned to receive twice-daily doses of 120 mg or 60 mg of tozadenant or placebo as an addition to their regular Parkinson’s medications for 24 weeks. The study’s goal is to determine the number of hours per day in which patients are in the “off” state.
Off time in Parkinson’s disease refers to periods of the day when the therapy patients are undergoing works less, causing a worsening of symptoms.
Tozadenant is an oral adenosine A2a receptor antagonist undergoing investigation as an adjuvant therapy to Parkinson’s disease patients treated with levodopa. Therapies that block A2a receptors, such as tozadenant, could become a new class of drugs, depending on patient outcomes, and the first approved in 20 years in the U.S. to improve motor symptoms in Parkinson’s disease.
https://parkinsonsnewstoday.com/2017/11/20/parkinsons-disease-acorda-adds-more-blood-cell-monitoring-tozadenant-trials-following-adverse-events/

NeuroExpresso: Web app enables exploration of brain cell types

November 20, 2017

Mouse brain cell type specific expression database compiled from publicly available datasets. Credit: Mancarci et al., eNeuro (2017)


An online database of gene expression profiles for 36 major types of brain cells from 12 brain regions, based on mouse data from multiple laboratories, is reported in a new paper published in eNeuro. The tool is provided as a resource for neuroscientists at neuroexpresso.org/ and will be presented on Wednesday November 15 at Neuroscience 2017, the annual meeting of the Society for Neuroscience.

Brain cells can be described in many different ways depending on qualities such as location, electrical properties and the neurotransmitters they release. Identifying specific  that are expressed by cells straddling these classifications can help to better define their functions and properties, which is necessary to understand their role in neurological disorders.
Paul Pavlidis and colleagues reanalyzed previously published data to create a comprehensive catalogue of brain cell type data in a web-based application called NeuroExpresso. The authors used the data to identify marker genes, which can be used to estimate cellular composition of mouse and human tissue using marker gene profiles. They demonstrate the agreement of their approach with experimental results from studies of human brain disorders including Parkinson's disease. An early version of NeuroExpresso has been used to interpret gene expression in the brains of suicide victims.
More information: Cross-Laboratory Analysis of Brain Cell Type Transcriptomes with Applications to Interpretation of Bulk Tissue Data, DOI: 10.1523/ENEURO.0212-17.2017 
Provided by: Society for Neuroscience 
https://medicalxpress.com/news/2017-11-neuroexpresso-web-app-enables-exploration.html