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Saturday, November 11, 2017

Mrs Europe launches campaign to raise awareness about Parkinson’s disease in Gibraltar

November 11, 2017

NOBLE: Baglietto hopes more people are aware of the disease

Davinia Baglietto, who was crowned Mrs Europe in 2017, is seeking to use her position to improve care for Parkinson’s patients in Gibraltar.
Baglietto is seeking to use her pageant platform to organise support groups and a day centre for those affected by the condition.
Parkinson’s disease is a long-term degenerative disorder of the motor system that typically affects those over the age of 60.
The cause is a personal one for Davinia, whose father was diagnosed with the disorder fifteen years ago.
“I entered Mrs Gibraltar with the purpose of raising awareness for Parkinson’s disease as there is not enough in Gibraltar to do with it,” she told the Gibraltar Olive Press.
“Gibraltar has supported me every sense of the way and I thought I need to give something back.”
While Davinia is extremely complimentary of the current services provided by the Gibraltar Health Authority, in particular those of the GHA physio department, she believes there needs to be more mental support for patients and their families.
“They are doing an extraordinary job but the number of patients is increasing.
“For me, there needs to be a bigger location so that patients can have their own space and have more regular support.”
Davinia said her mother acts as a full time carer for her father and currently only receives assistance from a professional for one hour a day.
“My father used to work three jobs when we were small, he used to be a police officer and you can only imagine it, going from being as physical as you can be to having to have assistance to even get into the bath,” she said.
“For them it is so demoralising, my mother will always look after him but she needs more mental health assistance for him from professionals who understand.”
Davinia believes a day centre for Parkinson’s disease would also allow families the opportunity to recover from taking care of their loved ones.
“I’m aware it is going to be a long road, but nothing worthwhile is easy,” Davinia concluded.
http://www.gibraltarolivepress.com/2017/11/11/mrs-europe-launches-campaign-raise-awareness-parkinsons-disease-gibraltar/

Smell Test Challenge Suggests Clinical Benefit for Some Before Development of Alzheimer’s

NEUROSCIENCE NEWS    NOVEMBER 10, 2017
Source: Columbia University Medical Center.

Summary: Columbia researchers have identified a way in which to determin if a patient with MCI may respond to cholinesterase inhibitors.

In this year-long study, 37 participants with MCI underwent odor identification testing with the University of Pennsylvania Smell Identification Test (UPSIT). The test was administered before and after using an atropine nasal spray that blocks cholinergic transmission. NeuroscienceNews.com image is for illustrative purposes only


Researchers at Columbia University Medical Center (CUMC) and the New York State Psychiatric Institute (NYSPI) may have discovered a way to use a patient’s sense of smell to treat Alzheimer’s disease before it ever develops. Having an impaired sense of smell is recognized as one of the early signs of cognitive decline, before the clinical onset of Alzheimer’s disease. The researchers at CUMC and NYSPI have found a way to use that effect to determine if patients with mild cognitive impairment may respond to cholinesterase inhibitor drugs to treat Alzheimer’s disease.

The findings were published online this week in the Journal of Alzheimer’s Disease.

Cholinesterase inhibitors, such as donepezil, enhance cholinergic function by increasing the transmission of the neurotransmitter acetylcholine in the brain. Cholinergic function is impaired in individuals with Alzheimer’s disease. Cholinesterase inhibitors, which block an enzyme that breaks down acetylcholine, have shown some effectiveness in improving the cognitive symptoms of Alzheimer’s disease. 

However, they have not been proven effective as a treatment for individuals with mild cognitive impairment (MCI), a condition that markedly increases the risk of Alzheimer’s disease.

“We know that cholinesterase inhibitors can make a difference for Alzheimer’s patients, so we wanted to find out if we could identify patients at risk for Alzheimer’s who might also benefit from this treatment,” said D.P. Devanand, MBBS, MD, professor of psychiatry, scientist in the Gertrude H. Sergievsky Center at CUMC, and co-director of the Memory Disorders Clinic and the Late Life Depression Clinic at NYSPI. “Since odor identification tests have been shown to predict progression to Alzheimer’s, we hypothesized that these tests would also allow us to discover which patients with MCI would be more likely to improve with donepezil treatment.”

In this year-long study, 37 participants with MCI underwent odor identification testing with the University of Pennsylvania Smell Identification Test (UPSIT). The test was administered before and after using an atropine nasal spray that blocks cholinergic transmission.

The patients were then treated with donepezil for 52 weeks, and were periodically reevaluated with the UPSIT and with memory and cognitive function tests. Those who had a greater decline in UPSIT scores, indicating greater cholinergic deficits in the brain, after using the anticholinergic nasal spray test saw greater cognitive improvement with donepezil.
In addition, short-term improvement in odor identification from baseline to eight weeks tended to predict longer-term cognitive improvement with donepezil treatment over one year.

“These results, particularly if replicated in larger populations, suggest that these simple inexpensive strategies have the potential to improve the selection of patients with mild cognitive impairment who are likely to benefit from treatment with cholinesterase inhibitors like donepezil,” said Dr. Devanand.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
The study is titled: “Change in Odor Identification Impairment is Associated with Improvement with Cholinesterase Inhibitor Treatment in Mild Cognitive Impairment.” The other contributors are Cody Lentz (CUMC), Richard E. Chunga (NYSPI), Adam Ciarlegilio (CUMC, NYSPI), Jennifer M. Scodes (Columbia’s Mailman School of Public Health), Howard Andrews (CUMC, Mailman), Peter W. Schofield (University of Newcastle, Callaghan, Australia), Yaakov Stern (CUMC), Edward D. Huey (CUMC), Karen Bell (CUMC), and Gregory H. Pelton (NYSPI, CUMC).

Disclosures

Dr. Bell owns stock in Baxter. Dr. Devanand has received consulting fees for serving on Astellas’ Scientific Advisory Board, Axovant’s Educational Advisory Board, Eisai’s Data Safety Monitoring Board, and Genentech’s Scientific Advisory Board, and has received grants from Avanir. Dr. Stern has received consulting fees from Lilly USA, LLC, Takeda Global Research & Development Center, Inc, and Axovant Sciences, Inc. The other contributors report no financial or other conflicts of interest.

Funding: This study was supported in part by the Department of Defense grant W81XWH-12-1-0142 and the National Institute on Aging (R01AG041795).
Source: Gregory Flynn – Columbia University Medical Center
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is for illustrative purposes only.
Original Research: The study will appear in Journal of Alzheimer’s Disease.

http://neurosciencenews.com/smell-test-alzheimers-7920/

Parkinson’s disease Antidepressant nortriptyline could slow Parkinson’s pathology

November 10, 2017    Clinical Pharmacist

The drug could be used as a multi-functional compound to treat comorbid depression in Parkinson’s disease and also slow down the progress of the disease, researchers say.



Source: Shutterstock.com
Study shows that the antidepressant nortriptyline could become a multi-functional compound to treat Parkinson’s disease 

One potential strategy for treating Parkinson’s disease is to prevent the formation of intracellular inclusions comprised of misfolded alpha-synuclein in the brain.
In a paper in Neurobiology of Disease (online, 12 July 2017), researchers explored the effect of the antidepressant nortriptyline on the formation of alpha-synuclein[1].
They first showed in vitro that the drug is able to bind directly to alpha-synuclein and interfere with its folding, inhibiting formation of toxic forms of the protein. In both in vitro and animal models they then showed that this led to reduced levels of accumulation, aggregation and neurotoxicity of alpha-synuclein.
Noting that nortriptyline is considered effective and safe for treating comorbid depression in Parkinson’s disease, the team suggested it could become a multi-functional compound to treat the disorder.

Friday, November 10, 2017

Replacing Cells in the Human Brain Could Bring an End to Parkinson’s Disease

by Ben Stecher on November 9, 2017

A group of iPS cells grown from human skin tissue at Osaka University

The following was written with Prof. Gerold Riempp, a professor of information systems who was diagnosed with Parkinson’s disease 16 years ago at age 36. He is co-founder of a charitable organization in Germany that supports the development of therapies that aim to cure PD.
The idea behind cell replacement therapy(CRT) for PD is pretty simple: lack of mobility in PD is the result of the dysfunction and death of a specific kind of cell in the midbrain. While there are a few other things that go wrong in PD, the progressive loss of motor skills is the biggest problem most diagnosed face. Since we are reasonably sure that this lack of mobility results from the impairment and death of dopamine producing cells in an area of the midbrain called the substantia nigra, why not try to replace those cells?
Replacing those cells is one of three core problems that each person diagnosed with PD needs to address. They are:
1. Keeping remaining cells healthy
Once diagnosed, most people have already lost production of 50-80% of dopamine in their midbrain. The problem then is to stop further disease progression by figuring out how to get rid of everything that might be harming the remaining 20-50% of cells while giving their body everything it needs to keep those cells alive and active.

2. Clearing clogged cells
Of those 50-80% of non-dopamine producing cells, a portion are still alive, they are just not doing their job, producing dopamine. This impairment is a result of a range of interrelated factors that harm the cells and eventually lead to their death. Most researchers believe the problem can be boiled down to the clumping of a misfolded protein called alpha-synuclein. Many different methods are being tried in labs around the world to clear these clumps and stop more from accumulating. But this might only be part of the story since a wide variety of other factors also lead to cell death.


3. Replacing dead cells
Then we come to what to do about all of those dead cells. A couple of different options are being considered to get the brain to stimulate the production of new neurons or replace the function of dead ones. However, the most promising therapy being developed is stem cell therapy, now commonly referred to as cell replacement therapy. It works by placing new dopamine producing neurons into the part of the brain where the dead neurons used to release dopamine.

If a patient manages to address problems one and two they might have no need for CRT. The reason for this is that he or she can likely rescue a considerable portion of the damaged but still living cells and thereby bring dopamine production back to a level that allows for normal movement. CRT will generally be for people who have had PD for a longer time and whose remaining healthy cells plus the rescued ones together are not capable of providing enough dopamine.

The late 80’s and 90’s saw a number of CRT trials for Parkinson’s disease with mixed results. But we now have a much better understanding of what kind of cells to use, how to culture and store those cells, how to implant them, and who this therapy would be best for.
We also now have iPS cells (induced pluripotent stem cells). Discovered in 2006, these are cells that have been chemically reprogrammed, usually from adult skin tissue, back into pluripotent stem cells. (Pluripotent means they are capable of becoming almost any cell in the body). Using these cells for transplantation has two major advantages. One, it eliminates the need for potentially harmful immuno-suppressors. Two, it has none of the ethical issues that come with using fetal stem cells. But iPS cells are much more expensive and technically difficult to produce.
Despite all the progress made, cell replacement therapy is still very controversial and fraught with all sorts of technical issues. Luckily, CRT for PD is one of the only fields of medical science where the top labs around the world are cooperating with each other. An international consortium of labs has come together under a name that sounds like it was ripped out of a Marvel comic, the GForce-PD. Each lab in the GForce-PD aims to bring CRT for PD to clinical trial within the next few years.
Infographic made by PhD neuroscientist Kayleen Schreiber at kayleenschreiber.com


The GForce-PD
New York City – Run by Dr. Lorenz Studer out of the Rockefeller research labs in New York City. Dr. Studer pioneered many of the reprogramming techniques being used around the world to convert pluripotent stem cells into dopamine producing neurons. His lab was recently announced to be part of a huge funding initiative from Bayer Pharmaceuticals to help speed up development of CRT. Studer’s lab is aiming to start transplantation of embryonic stem cells in human trials in early 2018.
Kyoto, Japan – Dr. Jun Takahashi’s lab in Kyoto is working on producing several iPS lines for the Japanese population. One advantage they have is the relative homogeneity of Japanese people allows them to use a dozen or so iPS lines for almost everyone in the country. The lab recently made headlines with results from monkey trials that showed human iPS cells graft safely, with no signs of malignant growth, two years after transplantation.
Cambridge, England – Dr. Roger Barker’s lab has been working on cell replacement therapy for Parkinson’s disease for a number of years through the Transeuro project. His lab is pushing forward with more embryonic stem cell transplantations expected to begin in 2020. They also work very closely with the team in Sweden.
Lund, Sweden –  The lab in Lund has been working on CRT for PD since the 80’s and has been part of a number of human trials. The lab is now run by Dr. Malin Parmar whose team has also pioneered many of the techniques used in direct programming that will one day allow researchers to skip the stem cell phase all together and produce dopamine cells directly in the brain.
San Diego, California – The team is moving rapidly towards iPS cell transplantation under Dr. Jeanne Loring at the Scripps research center. They are the only lab that uses patient’s own cells for transplantation. Another unique feature of this lab is that it has been a community funded initiative under the Summit For Stem Cells foundation.
Though there is a lot of excitement building around cell replacement therapy, we need to proceed carefully. The field has potential for setbacks from some of the less rigorous trials being conducted in places like Australia and China where regulatory standards are more lax. Researchers in these areas are already going ahead with trials that do not meet the standards set by the GForce-PD. These have the potential to put a black-eye on all cell replacement therapies.
Also, producing pure batches of dopamine neurons is still a highly technical process that only a few labs in the world are capable of doing safely and effectively. Thankfully a few other labs around the world are joining the efforts of the GForce-PD, such as Dr. Tilo Kunath’s lab in Edinburgh, which is working on techniques to better differentiate and characterize the cell lines used for transplantation.
The Future of Cell Replacement Therapy
These therapies being developed for Parkinson’s disease will, in essence, be version 1.0 of CRT. Clinical trials are set to begin next year and the therapy is expected to be widely available to people diagnosed with Parkinson’s disease within the next 5-10 years.
Version 2.0 will be CRISPR-modified, disease resistant grafts, with genetic switches to modulate dopamine production and graft size.
Version 3.0 will make use of an emerging field called in vivo direct programming where viruses are inserted into the brain and transform other existing cells into dopamine producing cells.
(Edit: Credit to Dr. Tilo Kunath for correcting versions 2.0 and 3.0)
Dopamine neurons grown from iPS cells at 40 times magnification, from the Gladstone Institute
CRT for PD is one of the most exciting areas of research on the planet. It is a powerful demonstration of the progress we as a species have made in our attempt to gain mastery over the forces of biology. It has the potential to improve the lives of the millions living with PD, and the millions yet to be diagnosed. Once the transplanted cells have connected with their surroundings and start delivering dopamine to the right places, it should allow patients to gradually reduce their medication. Being able to move normally and not deal with the side effects of all the drugs and other therapies is what PD patients around the world are dreaming of.
https://futurism.com/replacing-cells-human-brain-parkinsons-disease/

Biomarker may predict early Alzheimer's disease

November 10, 2017

DAG (green-labeled peptide) targeting to the brain blood vessel (labeled red) in the hippocampus of the Alzheimer brain. Credit: Ruoslahti Lab, SBP


Researchers at Sanford Burnham Prebys Medical Discovery Institute (SBP) have identified a peptide that could lead to the early detection of Alzheimer's disease (AD). The discovery, published in Nature Communications, may also provide a means of homing drugs to diseased areas of the brain to treat AD, Parkinson's disease, as well as glioblastoma, brain injuries and stroke.

"Our goal was to find a new biomarker for AD," says Aman Mann, Ph.D., research assistant professor at SBP who shares the lead authorship of the study with Pablo Scodeller, Ph.D., a postdoctoral researcher at SBP. "We have identified a peptide (DAG) that recognizes a protein that is elevated in the  of AD mice and human patients. The DAG target, connective tissue growth factor (CTGF) appears in the AD brain before , the pathological hallmark of AD."
"CTGF is a protein that is made in the brain in response to inflammation and tissue repair," explains Mann. "Our finding that connects elevated levels of CTGF with AD is consistent with the growing body of evidence suggesting that inflammation plays an important role in the development of AD."
The research team identified the DAG peptide using in vivo phage display screening at different stages of AD development in a mouse model. In young AD mice, DAG detected the earliest stage of the disease. If the early appearance of the DAG target holds true in humans, it would mean that DAG could be used as a tool to identify patients at early, pre-symptomatic stages of the disease when treatments already available may still be effective.
"Importantly, we showed that DAG binds to cells and brain from AD human patients in a CTGF-dependent manner" says Mann. "This is consistent with an earlier report of high CTGF expression in the brains of AD patients."

https://youtu.be/_I3CeUIVgq4
Dr. Aman Mann of the Sanford Burnham Prebys Medical Discovery Institute discusses a finding that may lead to earlier detection and treatment of Alzheimer's disease. Credit: Kristen Cusato

"Our findings show that endothelial cells, the cells that form the inner lining of blood vessels, bind our DAG peptide in the parts of the mouse brain affected by the disease," says Erkki Ruoslahti, M.D., Ph.D., distinguished professor at SBP and senior author of the paper. "This is very significant because the endothelial cells are readily accessible for probes injected into the blood stream, whereas other types of cells in the brain are behind a protective wall called the blood-brain barrier. The change in AD blood vessels gives us an opportunity to create a diagnostic method that can detect AD at the earliest stage possible.
"But first we need to develop an imaging platform for the technology, using MRI or PET scans to differentiate live AD mice from normal mice. Once that's done successfully, we can focus on humans," adds Ruoslahti.
"As our research progresses we also foresee CTGF as a potential therapeutic target that is unrelated to amyloid beta (Aβ), the toxic protein that creates brain plaques," says Ruoslahti. "Given the number of failed clinical studies that have sought to treat AD patients by targeting Aβ, it's clear that treatments will need to be given earlier—before amyloid plaques appear—or have to target entirely different pathways.
"DAG has the potential to fill both roles—identifying at risk individuals prior to overt signs of AD and targeted delivery of drugs to diseased areas of the brain. Perhaps CTGF itself can be a drug target in AD and other  disorders linked to inflammation. We'll just have to learn more about its role in these diseases".
This technology has been licensed to a startup company, AivoCode Inc.
Journal reference: Nature Communications 
https://medicalxpress.com/news/2017-11-biomarker-early-alzheimer-disease.html

This device will let you feel what it's like to suffer from Parkinson's

Christina Farr |   November 9, 2017




https://youtu.be/nBgG4ZVHoPc



Imagine actually feeling the symptoms of a loved one with a debilitating disease.
Soon you might be able to, with help of a device from Toronto-based design consultancy Klick Health. The team of doctors, engineers and designers came up with a way to mimic the feeling of having a Parkinson's tremor.
The device is not yet approved for the commercial market, and is still being tested in clinical trials. 
But when I tried it at a medical conference called Exponential Medicine in San Diego, I found the experience surprisingly painful and emotional.
What's particularly remarkable about it — and speaks to the broader goal of bringing more empathy to medicine — is that a user can request to feel the precise tremor of a loved one that they're caring for. The idea is that it will inspire a caregiver to feel a stronger personal connection to the person with the disease. "To have the exact symptoms mirroring the person across from you certainly has a level of empathy that's even greater than having a generalized symptom," said Gautam Gulati, the company's health innovator in residence and a physician, whose own father recently passed away from the disease.
Next up, Klick's team is looking at other diseases that involve changes to sensory experiences, including chronic respiratory conditions. The biggest hurdles involve convincing federal regulators that it's safe and effective, and figuring out whether clinicians, patients and caregivers would pay for it.
See see another video go to:
https://www.cnbc.com/2017/11/09/parkinsons-klick-health-device-lets-you-feel-symptoms.html

Thursday, November 9, 2017

FoxFeed Blog: Ask the MD: Weight Loss and Parkinson's Disease

 Posted by  Rachel Dolhun, MD, November 09, 2017



Weight loss in Parkinson's is common, but it's usually mild or, at most, moderate. Changes can occur at any time with Parkinson's disease (PD), but may be more likely in later phases. It's important to recognize and address weight loss because it could lead to malnutrition or exacerbate motor and non-motor symptoms.

Weight Loss Has Many Possible Causes 
It can be hard to pinpoint the exact reason your weight is dropping. You could need more calories than you realize. Some motor symptoms, such as rigidity and tremor, can increase your body's energy requirements. Dyskinesia (involuntary movements that can occur with long-term levodopa use) does the same. Motor symptoms also can make meal preparation or dining more challenging.

Non-motor symptoms can sometimes cause a person to eat less:
  • Smell loss or depression can lead to loss of appetite and decreased food intake; 
  • Constipation and slowed stomach emptying may cause nausea, abdominal bloating or a full feeling after consuming small amounts; and 
  • Swallowing problems might require a change in diet or make mealtimes difficult. 
Conditions other than Parkinson's also can bring weight loss. If you can't reach a stable weight despite addressing PD symptoms, consider other possibilities, such as overactive thyroid or, in some situations, cancer. It's often a good idea to have a thorough evaluation by your general medical doctor.

Work with Your Doctor to Manage Weight Loss 
Significant weight loss in PD is associated with a lower quality of life. This is because it can make it harder to control motor and non-motor symptoms, and increase risk of infection and bone loss (osteoporosis).

If you notice a shift in your weight, make sure you talk with your doctor. He or she can monitor your weight and together you can work to figure out the reason(s). Your physician may start by asking about changes in mood or eating habits, as well as difficulty with swallowing or constipation. There's no one-size-fits-all approach to manage weight loss, but a few tactics you might consider:
  • Adjust Parkinson's medications: Especially if dyskinesia is significant and thought to be a main contributing factor, your drug regimen may be tweaked.
  • Treat non-motor symptoms: If depression is decreasing appetite, your doctor may prescribe a medication to help boost mood. For swallowing problems, you may be referred to a speech therapist who can do a detailed evaluation and make appropriate diet recommendations.
  • Evaluate other conditions: Sometimes doctors look for other reasons for weight loss. They may draw blood to look at vitamin levels or thyroid function, or they might ask you to see your primary care physician for a full evaluation.
  • See a registered dietitian: In some cases, your doctor may refer you for a consultation with one of these experts, who can look at your current diet and help you optimize your calorie, protein and nutritional intake. 
As with every symptom that may accompany PD, weight loss doesn't occur in everyone. And, when it does, it happens to different degrees (i.e., mild in some and more significant in others). Management of weight loss is individualized and targeted to the underlying cause.

https://www.michaeljfox.org/foundation/news-detail.php?ask-the-md-weight-loss-and-parkinson-disease

OU Soundings Series to highlight importance community engagement

November 9, 2017

Oakland University’s popular Soundings Series will return on Monday, Nov. 27 with a special presentation by Ali Woerner, associate professor of dance and co-founder of “Take Root,” a contemporary dance company-in-residence at OU.


Oakland University’s popular Soundings Series, which features examples of faculty successfully taking their research out of the classroom and using it to make a positive difference in the world, will return on Monday, Nov. 27 with a special presentation by Ali Woerner, associate professor of dance and co-founder of “Take Root,” a contemporary dance company-in-residence at OU. 

The event will take place from 3-4:30 p.m. in 242 Elliott Hall. Woerner will be presenting information about Take Root’s Dance for Parkinson’s Disease Program, why it’s important and ways higher education can be used to improve the lives of others in the community. She will also be highlighting her own community engagement efforts in Oakland County.

“Community engagement is so important to what we’re doing,” she said. “It’s the way we started, and it’s the way we’ve survived. We let people know what’s going on. Not only that, but we get them to tell others about the program, or come to the class themselves. Sometimes the hardest part is just getting them in the room.”

Based on the Mark Morris Dance Group’s “Dance for PD” program, the Dance for Parkinson’s Disease program at Oakland University was developed to empower those living with Parkinson’s Disease (PD), as well as their caregivers, spouses and family members, to explore movement and music through a program that engages their minds and bodies in an enjoyable social environment.

“We try to give them a space that’s safe,” Woerner said. “That’s really important, especially for this group of people who are dealing with being vulnerable every minute of their lives. They worry about being able to cross the street in time, about getting to the phone when it rings, etc. It’s just a constant thing for them. To give them an hour where they don’t have to worry, where they can just have fun, it’s great. Sure, we talk about how the movements are going to help them physically, but we don’t harp on it. That’s not our purpose. We’re there to make them feel good.”

According to Woerner, the classes are currently offered in three locations in Oakland County:

  • Oakland University, 201 Meadow Brook Road, Rochester, Mich.

  • The Older Person’s Commission, 650 Letica Drive, Rochester, Mich.

  • St. Joseph Mercy Oakland, 44405 Woodward Ave., Pontiac, Mich.

“What I think is really interesting about this work is that the basis of it is dance, but it’s also dealing with a medical issue and a neurological disease,” Woerner said. “So it really cross-pollinates because you’re dealing with education, health sciences, nurses, physical therapy, dance therapy, music, etc. It’s really exciting because you’re touching all those groups. In fact, I think that’s why we’ve been as successful as we have been with the program.”

For more information about the Soundings Series, contact Leanne DeVreugd, program assistant for Women in Science, Engineering and Research (WISER), at ldevreug@oakland.edu, or visit the Soundings Series website at Oakland.edu/research/soundings-series.

https://oakland.edu/research/news/2017/ou-soundings-series-to-highlight-importance-community-engagement

ISMP Raises Safety Concerns for 2 Novel Agents

By Nikki Kean   November 9, 2017


The postmarketing safety record of two recently approved drugs with novel mechanisms of action has raised concerns, leading investigators to examine how these agents got approved in the first place, according to a Quarterwatchreport by the Institute for Safe Medication Practices (ISMP).

ISMP issued safety alertsfor pimavanserin (Nuplazid, ACADIA Pharmaceuticals) and the combination of sacubitril and valsartan (Entresto, Novartis) following reports of adverse event (AE) data “warranting careful consideration, and likely further action."

Pimavanserin and Hallucinations
The FDA approved pimavanserin in April 2016 for the treatment of hallucinations and delusions associated with Parkinson’s disease psychosis. Approximately 50% of patients with Parkinson’s will develop hallucinations and other forms of psychosis as the disease progresses, according to the ISMP report. This primarily is caused by the medications commonly used to treat Parkinson’s, namely, levodopa—typically given in combination with carbidopa—and dopamine agonists (e.g., pramipexole). 

Although most antipsychotic drugs primarily block normal signaling of the neurotransmitter dopamine, “pimavanserin acts to block signaling with an important subfamily of serotonin receptors (5 HT2A) that mediate memory, cognition, learning and numerous other body functions,” the report noted. Pimavanserin initially was indicated for a very specific side effect of Parkinson’s, but the drug now is “being tested for use in larger patient populations, including those with psychosis in Alzheimer’s, and as adjunct therapy in schizophrenia,” the ISMP report stated.
In the 12 months ending March 2017, 2,236 AEs were reported to the FDA Adverse Event Reporting System related to pimavanserin. The ISMP team looked at the most frequently reported AEs and divided them into four groups: hallucinations (21.8%), drug ineffective (14.9%), confusion (11.5%) and death (10.9%).
Further analysis provided additional evidence that AE reports of hallucinations likely were showing that the drug was making psychosis worse or was ineffective in some patients. “The number of reports of hallucinations was large [n=487], with 73% observed by health professionals, who could be expected to understand that hallucinations occur in 20% to 70% of Parkinson’s patients,” ISMP noted. 
The AE data mirrored results of the clinical trial of pimavanserin. In that study, “both hallucinations and confusional state also occurred more frequently as an adverse event in treated patients compared with those getting a placebo,” according to ISMP. 
A closer look at the FDA approval process revealed that pimavanserin was approved based on limited scientific evidence, the group noted. “[The approval] relied on a single clinical trial indicating a minimal treatment effect, used a measurement scale for symptoms that had not been validated, and succeeded only after three previous trials had failed to demonstrate a benefit. Further, the agency’s medical reviewer recommended against approval and was overruled.” 
According to ISMP, the reviewer “noted that although other psychiatric drugs were often approved on limited evidence of benefit, in the case of pimavanserin, [the] treatment more than doubled the risk of death and/or serious adverse events in its pivotal trial.”
ISMP found that the post-approval AE reports disclosed an additional safety issue: “We identified 318 cases where pimavanserin was combined with quetiapine (Seroquel [AstraZeneca]) or other antipsychotics that block dopamine signaling. These drugs are not recommended for use in the elderly and are not approved for use in Parkinson’s.”
ISMP noted that it shared its preliminary results with the manufacturer, ACADIA. The company responded by claiming that the large volume of AEs attributed to its drug were due in part “to the manufacturer’s extensive contact with health professionals and consumers through a specialty pharmacy network that distributed the drug, and because of a company patient support program,” the ISMP report stated. “[ACADIA] also said the reports of hallucinations might have occurred before the drug became fully effective approximately four weeks after treatment started.”
ISMP took issue with at least some of that reasoning. “While the company’s contacts with health professionals and consumers likely expanded the number of adverse event reports after product launch, these reports nevertheless reflect the experiences of health professionals and consumers in a real-life, post-market setting. 
The overall message in these adverse event reports is that hundreds of health professionals are trying this new drug with their patients and reporting that either it is not providing the expected benefit or [is] making some psychosis worse. The large number of deaths also remains a concern in a setting where increased mortality was at least suspected if not proven in the clinical trials.” 
ISMP urged the FDA and ACADIA to “consider additional warnings and other measures to deal with inappropriate combination therapy with antipsychotic drugs” such as pimavanserin.

Sacubitril-Valsartan and Hypotension
Sacubitril-valsartan was approved in July 2015. The agent targets a new pathway involved in the regulation of blood pressure and “appears to improve mortality and cardiovascular outcomes in heart failure patients with reduced ejection fraction,” according to the ISMP QuarterWatch report. It usually is administered in conjunction with other heart failure therapies, in place of an angiotensin-converting enzyme inhibitor or another angiotensin II receptor blocker.

Like pimavanserin, the combination therapy was approved with evidence from a single trial, in this case a 27-month trial involving 8,442 patients. The trial was stopped early because of reduced cardiovascular mortality: from 16.5% among patients taking enalapril to 13.3% among those taking the combination agent. However, according to ISMP, “only patients with the best chance of benefiting from the drug were selected for the trial after a six-week run-in period to ensure tolerance to the drug and eliminate those experiencing early adverse drug effects.”
 In that study, 24.4% of patients experienced a hypotension-related AE, which FDA reviewers noted was likely an underestimate, given that the trial was conducted only with patients already known to tolerate the drug without AEs serious enough to warrant discontinuation.
When reviewing the AE data, ISMP found that hypotension was the leading AE reported for sacubitril-valsartan during the 12 months ending in March 2017, with symptoms ranging from dizziness to blackouts. 
“We identified 1,684 adverse event reports indicating a hypotension-related event, more than with any other cardiovascular drug in this period,” ISMP reported. Morbidity associated with the AEs, which occurred in older patients (median age, 70 years), was “not severe in two-thirds of the cases,” but 69 deaths were reported, according to ISMP. “The patient population taking this drug is substantial, with prescription growth increasing an average of 38% per quarter,” the report noted.

“While Entresto had consistently positive results in its one large clinical trial, the adverse event data illustrate the importance of clinicians being alert to the risks of hypotension,” ISMP stated, recommending that the “FDA and the manufacturer review existing safety data to see what additional warnings and precautions, such as more gradual escalation of the dose to the recommended level, might help reduce the risk of this adverse effect.”
http://www.pharmacypracticenews.com/Clinical/Article/11-17/ISMP-Raises-Safety-Concerns-for-2-Novel-Agents-/45247

Study: Cannabis May Treat Parkinson’s Disease and Other Movement Disorders

November 9,  2017    by Anthony Martinell

Cannabis have be an effective treatment option for those with Parkinson’s disease and other movement disorders, according to a new study published in the journal Molecular Psychiatry.






“Cannabis and related compounds have recently been studied as promising therapeutic agents in treatment of neurodegenerative and movement disorders including Parkinson’s disease”, begins the study’s abstract. “In this review we have examined the potential benefits of medical marijuana and cannabinoids in the treatment of both motor and nonmotor symptoms as well as in slowing the progression of the disease. We have looked into any scientific evidence that indicates the potential use of marijuana and/or related compounds for the treatment of PD.”
According to researchers; “Current treatments of PD provide only relief of motor symptoms and are associated with adverse effects such as dyskinesia. In addition, these therapies do not slow the progression of the disease.” Therefore, “there is an urgent need for safer drugs that can treat both motor and nonmotor symptoms of PD as well as drugs that slow the progression of the disease.”
The study states that research studies “have provided evidence for the potential effectiveness of medical marijuana and its components in the treatment of PD as cannabinoids act on the same neurological pathway that is disrupted in Parkinson’s disease. Involvement of the endocannabinoid system in the regulation of motor behavior, the localization of the cannabinoid receptors in areas that control movement, and the effect of cannabinoids on motor activity indicate that cannabinoids can be potentially used in the treatment of movement disorders.”
Researchers claim that cannabis “has been shown to improve nonmotor symptoms of PD such as depression, pain, sleep, and anxiety. Moreover, components of cannabis have been demonstrated to have neuroprotective effect due to their anti-inflammatory, antioxidative, and antiexcitotoxic properties.”
The study concludes that; “Due to combination of the above mentioned beneficial effects, cannabis may provide a viable alternative or addition to the current treatment of Parkinson’s disease.”

https://thejointblog.com/study-cannabis-may-treat-parkinsons-disease-movement-disorders/