Skin Test May Shed New Light on Alzheimer’s and Parkinson’s Disease

April 2, 2015 9:00 

New research has determined that a simple skin biopsy may be able to detect physical indicators of both Parkinson’s and Alzheimer’s disease. Researchers from the University of San Luis Patosi in San Luis, Mexico are presenting their study at the American Academy of Neurology’s 67th Annual Meeting. Using skin biopsies from both healthy individuals and those with various neurological diseases, researchers found that those with Parkinson’s possessed seven times the typical amount of tau proteins while those with Alzheimer’s presented eight times the usual amount of alpha-synuclein protein. “More research is needed to confirm these results, but the findings are exciting because we could potentially begin to use skin biopsies from living patients to study and learn more about these diseases. This also means tissue will be much more readily available for scientists to study,” said the lead researcher of the study. “This procedure could be used to study not only Alzheimer’s and Parkinson’s, but also other neurodegenerative diseases.” To learn more about this study:

Skin Test May Shed New Light on Alzheimer’s and Parkinson’s Diseases

Released: 12-Feb-2015 10:20 AM EST Citations

AAN Annual Meeting, April 2015

Newswise — WASHINGTON, D.C. – 

Scientists have discovered a skin test that may shed new light on Alzheimer’s and Parkinson’s diseases, according to a study released today will be presented at the American Academy of Neurology’s 67th Annual Meeting in Washington, D.C., April 18 to 25, 2015. 

The study showed that skin biopsies can be used to detect elevated levels of abnormal proteins found in the two diseases. 

“Until now, pathological confirmation was not possible without a brain biopsy, so these diseases often go unrecognized until after the disease has progressed,” said study author Ildefonso Rodriguez-Leyva, MD, at Central Hospital at the University of San Luis Potosi in San Luis Potosi, Mexico. “We hypothesized that since skin has the same origin as brain tissue while in the embryo that they might also show the same abnormal proteins. This new test offers a potential biomarker that may allow doctors to identify and diagnose these diseases earlier on.”

For the study, researchers took skin biopsies from 20 people with Alzheimer’s disease, 16 with Parkinson’s disease and 17 with dementia caused by other conditions and compared them to 12 healthy people in the same age group. They tested these skin samples to see if specific types of altered proteins were found—ones that indicate a person has Alzheimer’s or Parkinson’s. 

As compared to healthy patients and ones with dementia caused by other conditions, those with both Alzheimer’s and Parkinson’s had seven times higher levels of the tau protein. People with Parkinson’s also had an eight times higher level of alpha-synuclein protein than the healthy control group.

Alzheimer’s disease is ranked as the sixth leading cause of death in the United States, and 5.4 million Americans are currently diagnosed with Alzheimer’s disease. Parkinson’s disease affects one million Americans, with at least 60,000 new cases reported annually each year.

“More research is needed to confirm these results, but the findings are exciting because we could potentially begin to use skin biopsies from living patients to study and learn more about these diseases. This also means tissue will be much more readily available for scientists to study,” said Rodriguez-Leyva. “This procedure could be used to study not only Alzheimer’s and Parkinson’s, but also other neurodegenerative diseases.”

The study was supported by the National Council of Science and Technology of Mexico. 

Learn more about Alzheimer’s and Parkinson’s diseases at www.aan.com/patients. 

The American Academy of Neurology, an association of more than 28,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer’s disease, stroke, migraine, multiple sclerosis, brain injury, Parkinson’s disease and epilepsy

http://www.aansneurosurgeon.org/2015/04/02/skin-test-may-shed-new-light-on-alzheimers-and-parkinsons-disease/

Patient's own skin cells may hold key to new treatments for neurological diseases

Published on March 31, 2015 at 1:52 PM 

A patient's very own skin cells may hold the key to new treatments and even cures for devastating neurological diseases. A generous $1 million donation from Mr. J. Sebastian van Berkom, and critical partnerships with Brain Canada, Laval University, Marigold Foundation and the FRQS-Réseau Parkinson Quebec are driving an innovative, iPSC (induced pluripotent stem cell) research platform that will transform research into Parkinson's and other neurological diseases.

Millions of Canadians are affected by diseases of the brain such as ALS, Parkinson's and brain tumours, for which there are limited treatments and no cures. By 2020, neurological conditions will become the leading cause of death and disability. "Everyone's lives are touched in some way by neurological disease, says Mr. van Berkom, President of Van Berkom and Associates Inc." In creating The van Berkom Parkinson's Disease Open-Access Fund, I hope to change lives and support new research that will lead to new treatments and one day cures. The iPSC platform is a new paradigm for neuroscience research and as one of the world's great neuroscience centres, The Neuro is the place to drive it forward."

"This is the ultimate bench to bedside paradigm, from patient to the bench, back to the patient," says Dr. Guy Rouleau, Director of The Neuro. "With a unique interface between fundamental and clinical research, The Neuro is uniquely positioned to be a central hub in the iPSC platform. Partnering with Mr. Van Berkom, a generous and visionary philanthropist, propels The Neuro toward the goal of significantly deepening insight into disease mechanisms with unprecedented efficiency."

Patients' skin cells will be reprogrammed into induced pluripotent stem cells (iPSCs) at Laval University, under the leadership of Dr Jack Puymirat, and then differentiated at The Neuro into disease relevant cells for research. For example, in the case of Parkinson's this could be dopamine neurons. The cells can also be genome-edited, a state-of-the-art technique that can introduce or correct disease associated mutations - creating the most accurate disease models. These iPSCs will be made widely and openly available to researchers across Quebec for neuroscience research. This open-access approach exponentially increases the likelihood of breakthroughs in neurological disease.

"The unique and exciting aspect of this platform is that we are creating the most specific cells for studying disease using the patient's own tissue, which has distinct advantages over using generic cells or animal models," says Dr. Edward Fon, neurologist and co-Director of the Quebec iPSC platform. "Disease models using human samples are increasingly shown to be far more efficacious in trials, as they much more accurately mimic the disease condition. In the iPSC platform, not only can specific mutations be introduced but, cells are from patients' whose specific clinical history and genetic profile are known, a first step on the road toward neurological personalized medicine. The Neuro has access to a large and well-characterized patient population, who can help create a rich clinically-and genetically-derived registry and biobank. The initial targets in the platform will be ALS and Parkinson's disease (PD), using dopamine neurons for PD and both motor neurons and astrocytes for ALS."

Source:

McGill University

http://www.news-medical.net/news/20150331/Patients-own-skin-cells-may-hold-key-to-new-treatments-for-neurological-diseases.aspx

APRIL IS PARKINSON'S AWARENESS MONTH

Number of People With Parkinson's Disease Set to Double by 2031 

/EINPresswire.com/ -- Every day 10 people are diagnosed with Parkinson's disease. Over the next 16 years, the number of Canadians diagnosed with Parkinson's is expected to double to more than 163,700 and Parkinson Society Canada will be here for them. These statistics tell only part of the story. A recent Public Health Agency of Canada (PHAC) report MAPPING CONNECTIONS: An Understanding of Neurological Conditions in Canada, offers other data, details and insights about the impact of Parkinson's disease in Canada. It also shines a light on the magnitude of challenges faced by families who live with neurological conditions as a part of daily life. 

The health care costs of the disease are staggering. Parkinson's has the third highest direct healthcare costs of neurological conditions annually at $120,358,000, second to epilepsy and Alzheimer's and other dementias. For individuals living with Parkinson's disease, household finances can also suffer. People with Parkinson's have the highest rate of prescription drug use among those with neurological conditions and their annual out-of-pocket expenses average $1,100, second only to those people with spinal cord injuries.

"The impact on individuals and families can be overwhelming," says Joyce Gordon, President & CEO of Parkinson Society Canada."

Most caregivers are family members and caregiver stress doubles when caring for an individual with a neurological condition. This is particularly the case if the condition is accompanied by cognitive impairment or behavioral issues, which are common in people with Parkinson's. Fifty per cent of people living with Parkinson's experience memory limitations and 40 per cent experience thinking and problem-solving limitations.

Parkinson Society Canada will continue to extend its reach and ensure that every new person diagnosed with Parkinson's disease can find meaningful help and resources close to home. A new, interactive map has been launched that enables Canadians to find and connect to resources in their province so that they can live life to the fullest. This online tool complements the toll-free National Information and Referral Centre, which can be accessed at 1-800-565-3000. 

"It's important following a diagnosis of Parkinson's that individuals have access to evidence-based resources, which complement the information they've just received from their neurologist and family physician," says Grace Ferrari, National Manager, Professional & Public Education.

"It may be many months before their next specialist appointment, and in the meantime, they may have unanswered questions. We are here to make the journey more understandable."

Parkinson's is a chronic, degenerative neurological disease characterized by a loss of dopamine in the brain. There is no known cause or cure. Symptoms include: resting tremor, slowness of movement, stiffness or rigidity of muscles, difficulty with balance and walking, changes in voice volume and speech, and difficulty with fine movements. Non-motor symptoms include depression, loss of sense of smell, sleep disturbances and cognitive changes. The average age of onset is 60, but it can affect people as young as 30 or 40. 

For 50 years, Parkinson Society Canada (PSC), together with a network of partners across Canada, has provided education and supportive services for individuals, families and health professionals, while advocating for changes in health policies. Parkinson Society Canada's National Research Program has invested more than $24 million in more than 450 research projects to unlock the mysteries of Parkinson's disease. 

To find out more about Parkinson's disease programs and services available near you, call 1-800-565-3000 or visit www.parkinson.ca. Join the conversation on Twitter @ParkinsonCanada and follow Parkinson Society Canada on Facebook.

Reference:Neurological Health Charities Canada (NHCC), Health Canada, Public Health Agency of Canada (PHAC), Canadian Institute of Health Research (CIHR). MAPPING CONNECTIONS: An Understanding of Neurological Conditions in Canada. September 2014. 

For further information, contact:

Kelly Mills
Communications Associate
Parkinson Society Canada
1-800-565-3000, ext. 3469
kelly.mills@parkinson.ca

NeuroDerm to Announce Updated Topline Results of Phase II Study of Continuous, Subcutaneously-Delivered Levodopa/Carbidopa for the Treatment of Parkinson's Disease at the 67th Annual Meeting of the American Academy of Neurol

REHOVOT, Israel, April 1, 2015 (GLOBE NEWSWIRE) -- NeuroDerm Ltd. (Nasdaq:NDRM), a clinical stage pharmaceutical company developing drugs for central nervous system (CNS) diseases, announced that updated results from the Phase II Study assessing the safety, tolerability and pharmacokinetics (PK) of ND0612L will be presented at the American Academy of Neurology (AAN) 67th Annual Meeting taking place April 18 to 25, 2015 in Washington, DC.

ND0612L is the low-dose product candidate of NeuroDerm's proprietary liquid Levodopa/Carbidopa (LD/CD) formulation that provides continuous, subcutaneously-delivered treatment for patients with moderate to severe Parkinson's disease.

The company previously announced positive topline results of the study at The Michael J. Fox Foundation's 2014 Parkinson's Disease Therapeutics Conference in October 2014. The data showed that patients with moderate to severe Parkinson's disease who received continuous, subcutaneous doses of ND0612L exhibited clinically significant reduction in fluctuations of plasma levodopa concentrations compared to patients receiving placebo. Patients receiving ND0612L also experienced a corresponding in-clinic two-hour reduction over placebo in "off" time, improved sleep, better quality of life and global clinical improvement without an increase in troublesome dyskinesia.

The poster (P1.187), "Pharmacokinetics and Safety of ND0612L (LD/CD for Subcutaneous Infusion): Results from a Phase II Study in Moderate to Severe Parkinson's Disease," will be on display during Poster Session I - Movement Disorders: Parkinson's Disease Pharmacotherapy from 2:00 to 6:30 PM EDT on Monday, April 20. Lead investigator Nir Giladi, MD, Associate Professor in the Sackler Faculty of Medicine at Tel Aviv University and Chairman of the Department of Neurology at the Tel Aviv Sourasky Medical Center and Sheila Oren, MD, Vice President of NeuroDerm Clinical and Regulatory Affairs will be available to answer questions on the findings of the poster from 5:00 PM to 6:30 PM EDT.

About Levodopa

Oral administration of LD/CD is regarded as the "gold standard" treatment for patients suffering from Parkinson's disease. Levodopa crosses into the brain and converts into dopamine to complement the reduced brain-dopamine levels. Virtually all patients diagnosed with Parkinson's disease will require levodopa at some point over the course of their treatment for the disease, and 70% to 80% of patients receive the drug at any given point in time. However, levodopa is limited by its short half-life. Approximately three to four hours after a single dose, almost none of the drug remains in the plasma. In addition, levodopa suffers from low absorption when administered orally, with only about 30% of the levodopa entering the blood stream.

ND0612H, ND0612L

ND0612H and ND0612L are designed to significantly reduce motor complications in Parkinson's disease patients through continuous, subcutaneous delivery of LD/CD, maintaining steady, therapeutic levodopa plasma concentrations both day and night. ND0612H is intended to provide an alternative to surgical treatments associated with serious side effects that are currently offered to patients with severe Parkinson's disease.

About Parkinson's Disease

Parkinson's disease is a progressive neurodegenerative illness characterized by reduced dopamine in the brain, resulting in a debilitating decrease in the patient's motor and non-motor functions. Its symptoms, such as trembling in the extremities and face, slowness of movement and impaired balance and coordination, worsen over time and gravely impact the patient's quality of life. As the disease progresses, these symptoms become more severe, resulting in debilitating periods of decreased motor and non-motor functions, also referred to as "off" time. In addition, mainly as a result of excessive/intermittent oral doses of levodopa aimed at treating the "off" time, some patients experience involuntary movements, or dyskinesia. The "off" time and dyskinesia affect the majority of Parkinson's disease patients and interfere with day-to-day functions, causing patients to become severely disabled. Continuous administration of levodopa has been shown to effectively treat motor fluctuations in Parkinson's disease patients, however, a convenient route of continuous administration has not been introduced to date.

About NeuroDerm

NeuroDerm is a clinical-stage pharmaceutical company developing central nervous system (CNS) product candidates that are designed to overcome major deficiencies of current treatments and achieve enhanced clinical efficacy through continuous, controlled administration. In Parkinson's disease, the company has four product candidates which offer a solution for almost every Parkinson's disease patient from moderate to the very severe stage of the disease. The company has developed a line of levodopa-carbidopa (LD/CD) product candidates administered through a small belt pump that delivers a continuous, controlled dose of LD/CD. The LD/CD line of product candidates includes: ND0612L and ND0612H, delivered subcutaneously, for moderate and for advanced Parkinson's disease patients, respectively, and ND0680 for a subset of severe Parkinson's disease patients whose symptoms have advanced to a more acute stage, requiring even higher doses of LD/CD. In addition, NeuroDerm is developing ND0701, a novel subcutaneously delivered apomorphine formulation for patients who suffer from severe Parkinson's disease and who do not respond well to LD/CD. NeuroDerm is headquartered in the Weizmann Science Park, Rehovot, Israel.

Forward-Looking Statements

This press release contains forward-looking statements, within the meaning of the safe harbor provisions of the Private Securities Litigation Reform Act of 1995, that involve risks and uncertainties. Such forward-looking statements may include projections regarding our future performance and may be identified by words like "anticipate," "assume," "believe," "continue," "could," "estimate," "expect," "intend," "may," "plan," "potential," "predict," "project," "future," "will," "seek" and similar terms or phrases. The forward-looking statements contained in this press release are based on management's current expectations and projections about future events. There are important factors that could cause our actual results, levels of activity, performance or achievements to differ materially from the results, levels of activity, performance or achievements expressed or implied by the forward-looking statements. In particular, you should consider the risks provided under "Risk Factors" in our prospectus filed with the Securities and Exchange Commission on November 13, 2014. Any forward-looking statement made by us in this press release speaks only as of the date hereof. Factors or events that could cause our actual results to differ may emerge from time to time, and it is not possible for us to predict all of them. We undertake no obligation to publicly update any forward-looking statements, whether as a result of new information, future developments or otherwise.

CONTACT: NeuroDerm Contact:
         Oded S. Lieberman, PhD, MBA, CEO
         oded@neuroderm.com
         Tel.: +972-8-946 2729
         Cell: +1-617-517 6077
         
         U.S. Investor Contact:
         David Carey
         Lazar Partners Ltd.
         dcarey@lazarpartners.com
         +212-867-1762
         
         U.S. Media Contact:
         Hollister Hovey
         Lazar Partners Ltd.

         hhovey@lazarpartners.com

http://health.einnews.com/article/257858896/pkWLg_uMbjATpvt1

Vibrating pen makes it easier for Parkinson's patients to write

The ARC pen pictured above might look laughably large, but it could be the perfect option for folks with Parkinson's disease. It was created by a group of students from UK's Royal College of Art and the Imperial College London to combat a Parkinson's symptom called micrographia. That's characterized by a patient's handwriting becoming smaller and more cramped as they go along, to the point that it's not readable anymore. This pen prevents that from happening by stimulating key muscles through vibration (it's equipped with motors to make that happen), giving users more control over their hands. Further, its large size makes it more comfortable to hold than regular pens.

The team led by Lucy Jung started this project with something else in mind: they wanted to create a vibrating pen that can give non-patients a taste of what it feels like having to write with Parkinson's. Instead, they found that vibration enables larger and more legible handwriting, which really isn't that surprising. Remember Google X's vibrating spoon moonshot? That one allows patients to feed themselves without spilling anything, because vibrations counter the user's hand tremors. In fact, Jung and her team plan to equip other tools, such as makeup brushes and computer mice, with vibrating motors in the future.

http://health.einnews.com/article/257639190/ObfvVk0Z2OJaYjeb

10 Ways to Treat Depression Without Antidepressants

By: Sarah Landrum

You’ve probably been told that antidepressants correct the chemical imbalance in your brain. As it turns out, that’s not quite true. In fact, antidepressants might be doing you more harm than good.

Even if antidepressants do work, the fact remains that they’re insanely expensive. Considering how depression treatments can last a lifetime, it’s impractical to spend something like $21 to $1,000 a month just to keep the blues under control. Depression is already a burden enough by itself, without all the financial consequences that come with it.

It’s better to view antidepressants as a last resort, and try some – or all – of these alternative treatments first.

1. Practice Mindfulness

When you’re depressed, negative thoughts pour into your mind like water from a broken dam. You become paralyzed by fear and helplessness, because you feel like nothing can keep those thoughts under control.

Nothing – except meditation.

“In the group work that I’ve done with sufferers of anxiety or depression, I’ve found (mindfulness meditation) very beneficial because it calms the mind,” says psychologist Katie Sparks. That’s because you’re purposefully limiting your attention to the present moment, which helps you see things in a different – and more positive – light. So the next time you feel like beating yourself up again, take out a comfortable mat, sit on it in a lotus position and say ohm.

2. Laugh

Then again, maybe being an almost-Buddhist isn’t your thing. Maybe you’d rather do something that lifts your spirits within seconds, rather than something that takes several weeks to work.

In that case, try exposing yourself to funny TV shows/movies/books/what-have-yous. As it turns out, laughter really is the best medicine. It doesn’t matter if what makes you laugh is childish or stupid or weird. What matters is you get your daily recommended dosage of hilarity.

3. Don’t Isolate Yourself

Depression is a manipulative and malicious little monster. Every day, it sits on your shoulder, and whispers in your ear about how worthless you are and how you don’t deserve to be anywhere near the rest of society.

Don’t listen to it.

“In depression, social isolation typically serves to worsen the illness and how we feel,” says Stephen Ilardi, PhD, an associate professor of psychology and author of “The Depression Cure.” Apparently withdrawing from social interactions increases the brain’s stress responses. So, keep in touch with the people who matter to you, and don’t hesitate to let them know if you need their help.

4. Cut Toxic People Out of Your Life

On the flip side, you’re not doing yourself any favors by hanging out with people who dismiss your depression as something to snap out of. That makes about as much sense as mentally shrinking your rogue cells when you have cancer, or draining your blood sugar levels when you have diabetes.

To quote Deborah Serani, Psy.D, author of Living with Depression. “Part of living with depression requires you to learn how to reframe negative thoughts into positive ones, so having people in your life that are affirmative, nurturing and accepting of who you are will help ground you in a better healing environment.”

5. Consider Alternative Drugs

Granted, you have to be careful with cannabis and psilocybin. Both of them may have antidepressant properties, but both of them also have the potential to become drugs that worsen mental illness. Try them if you have no other option, but do remember to take the necessary precautions.

6. Eat the Right Foods

We’ve talked about how vitamin D can alleviate depression, dementia and diabetes. But there are othernutrients that keep depression at bay as well, including amino acids, folate, iodine, iron, magnesium, omega-3 fatty acids, selenium, vitamin B complex and zinc. Thankfully, many of these nutrients are in the foods you eat every day.

As for the foods you shouldn’t eat every day, avoid alcohol, caffeine, artificial sweeteners, hydrogenated oils, processed food, refined sugars and sodium-rich foods. All of these can wreak havoc on your nervous system, destabilize your blood sugar levels and/or damage your brain, among others.

7. Consider Acupuncture

According to a study published in Obstetrics & Gynecology, acupuncture can help alleviate depression. When the researchers administered depression-specific acupuncture on 150 pregnant women, 63 percent saw their symptoms improve. Although more tests have to be done to arrive at a definite conclusion, there’s no denying the promise shown in the study. Even if you’re not expecting, you may benefit from acupuncture.

8. Get Up and About

To be fair, depression does zap you of every bit of energy left in your body. However, exercise is still worth a try, since it has been proven to work just as well as – if not better than – antidepressants. No one knows exactly why this is, although the release of endorphins and norepinephrine during exercise might have something to do with it.

9. Grow a Garden

Can’t bring back your passion for your old hobbies? Try your hand at gardening. As we’ve reported before, gardeners are generally happier than non-gardeners. I suppose literally reaping what you sow brings out all these positive feelings buried deep inside you – no pun intended. Also, you have the benefit of getting fresh, uncontaminated vegetables right in your own backyard.

Don’t fret if gardening isn’t your thing. As long as your new hobby is meaningful and relaxing for you, it doesn’t matter what it is.

10. Volunteer for a Cause You Believe in

At some point, talking about depression with people you already know won’t be enough. You’re going to want to reach out of your established social circle and seek out the company of others. That’s a good sign.

Seek out organizations whose missions speak to you, and volunteer your services for them. Who knows; you might just reduce your depression symptoms, boost your well-being, and reduce your risk of dying by 22 percent.

Bonus: Don’t Stop Fighting

Here’s the thing about depression: You might have to fight it for the rest of your life. That’s because it has a nasty habit of sneaking up on you, and roundhouse-kicking you in the face when you least expect it. That said, if you’re able to cope with it using the tips above, you’ll always be able to roundhouse-kick it right back.

About the Author

Sarah Landrum is a freelance writer and health enthusiast sharing advice on living a happy and healthy life. She is also the founder of Punched Clocks, a career development site that helps professionals find happiness and success in their careers. Follow Sarah for more advice @SarahLandrum.

*This article was originally featured at Waking Times and was used here with permission.

http://themindunleashed.org/2015/03/10-ways-to-treat-depression-without-antidepressants.html

Q-and-A with 23andMe Parkinson’s Community Lead

FoxFeed Blog

Posted by  Maggie McGuire, March 25, 2015

Paul Cannon, PhD, leads the 23andMe Parkinson's Community.

Genetic testing company 23andMe made headlines recently with announcements first of a deal with pharmaceutical company Genentechand then of its own new Therapeutics Group.

The Michael J. Fox Foundation has a long-standing relationship with 23andMe, helping recruit members for its Parkinson’s Community study and collaborating on research projects such as our LRRK2 Cohort Consortium.

Paul Cannon, PhD, who leads the 23andMe Parkinson’s Community, spoke with us about the company’s recent news and what it means for Parkinson’s disease (PD) drug development.

MJFF: What can you tell us about the 23andMe partnership with Genentech?

Paul Cannon: The deal with Genentech is a collaboration to whole genome sequence approximately 3,000 individuals with Parkinson’s or with a first-degree relative with PD. (The ratio is yet to be determined.) It’s a unique opportunity to learn more about the genetics of people with Parkinson’s disease and hopefully identify novel targets and biological pathways.

MJFF: How can genomic sequencing lead to new targets and treatments?

PC: It’s obviously the start of a long process, but one of the principle aims is to discover new therapeutic targets for Parkinson’s disease and specifically for disease-modifying therapies. There are a number of interesting therapies in development, but we need more shots on goal.

Through whole genome sequencing, we’ll look for genetic variants such as small deletions or insertions that are difficult to detect with our present mapping-based approach. It’s a more thorough interrogation of the genome made feasible by the decreased cost of whole genome sequencing and the analysis methods that have come along hand-in-hand.

MJFF: What is the difference between genomic sequencing and what you get from the 23andMe spit test?

PC: In whole genome sequencing you’re interrogating the majority of a person’s genome [complete DNA sequence]: every position of the approximately 3 million base pairs that we have in our genome. The single nucleotide polymorphism [SNP pronounced SNIP] genotyping that 23andMe traditionally uses currently interrogates around 650,000 markers on the genome. Those are the mileposts, where sequencing looks at every section of the road.

MJFF: How can people with Parkinson’s disease get involved?

PC: For this study, we’ll be recruiting from the existing 23andMe Parkinson’s Community. We’re defining the genetic and clinical profiles that will give us the highest chance of success, and those individuals will be invited from the existing database.

That said, we encourage those not yet in the 23andMe Parkinson’s Community to join us. There will definitely be future projects; this won’t be our only effort.

MJFF: Speaking of other efforts, 23andMe recently launched its own Therapeutics Group. What can you tell us about the aims there?

PC: It’s very exciting to have the opportunity to work with an in-house team that is focused on development of therapeutics. We’ve obviously worked with commercial partners on drug discovery, and we’ll continue to do so. I’m hoping to work with them on potential projects for Parkinson’s research, but that’s still to be determined.

I can’t speak for them, but they’ll mine interesting data, presumably, and look for opportunities that pop out across the broad spectrum of diseases represented in 23andMe. They’re using human genetics to drive therapeutic discovery and to improve development of drugs by matching patients with the right drugs through the use of genetics.

MJFF: Thanks for your time, Paul. Anything else you want our audience to know?

PC: My pleasure. As a last note, I’d just say that we continue to look to work with partners across the Parkinson’s disease research community. There are opportunities for other collaborations and projects, and we’ll work together to continue to push forward Parkinson’s research, ultimately for a cure.

Learn more about the 23andMe Parkinson’s Community.

https://www.michaeljfox.org/foundation/news-detail.php?and-with-23andme-parkinson-community-lead

Technology designed for aerospace could improve Parkinson's therapy

When Rice University chemist Matteo Pasquali set out to to create strong and conductive carbon nanotube fibers, he had aerospace applications in mind. But it turned out his microscopic fibers are also great at communicating with the brain, making them an ideal candidate for therapies that deal with neurological disorders such as Parkinson's disease. Pasquali said: "...once we [he and his team] had them in our hand, we realized that they had an unexpected property: They are really soft, much like a thread of silk. Their unique combination of strength, conductivity and softness makes them ideal for interfacing with the electrical function of the human body."

At the moment, hard metal electrodes are implanted into the brain for Parkinson's therapy (they deliver electrical signals to calm tremors), but they're not actually that compatible with the organ's soft tissues. These flexible fibers are more biocompatible -- they're also cheaper and maintain better electrical connection. Plus, the scientists' tests prove they cause little inflammation and are as stable as commercial platinum used on electrodes.

Rice U assistant professor Caleb Kemere who studies Parkinson's disease believes these fibers could lead to self-regulating treatment devices for patients. Those devices will be able to read signals from the brain, analyze the best amount of electrical stimulation needed to calm tremors on a case-by-case basis and automatically administer jolts of electricity. That's the gist of it anyway: if you want to read the team's study in greater detail, bust out your science jargon decoder and check out the paper on ACS Nano

http://www.engadget.com/2015/03/27/carbon-nanotubes-parkinsons-therapy/

Alzheimer’s Drug Shows Promise in Slowing Disease

FoxFeed Blog

Posted by  Maggie McGuire, March 23, 2015

On Friday morning our CEO sent around an email. Subject: This is big!

He was sharing news from pharmaceutical company Biogen Idec(renamed today as simply Biogen) around an Alzheimer’s drug in development with strong implications for Parkinson’s research. The drug — aducanumab (BIIB037) — showed safety and positive impact not only on clinical symptoms but also on brain imaging scans.

Alzheimer’s, like Parkinson’s, is a disease of protein clumps. In Alzheimer’s the protein amyloid-beta aggregates into what scientists call plaques. In Parkinson’s disease (PD), alpha-synuclein protein clumps to form Lewy bodies. Researchers believe these plaques and Lewy bodies harm brain cells.

Biogen compared BIIB037 to placebo in 166 people in the early stages of Alzheimer’s disease. Analysis showed no change in plaques among those given the placebo, but there was significant change in those who received the drug. In fact, those given more of the drug showed greater decrease in plaques and less decline in cognitive and functional abilities.

Big news, indeed. The company is planning a Phase III study with hopes to begin later this year.

What does this mean for people with Parkinson’s disease?

While not everyone with Parkinson’s develops dementia, some do. People with PD dementia often have amyloid plaques like those seen in Alzheimer’s, so a drug such as BIIB037 may benefit that population, though further testing would be necessary.

These findings are a win for Parkinson’s research, too, because BIIB037 is an antibody (disease fighters that help the body fend off harmful substances). Scientists are currently testing two antibody approaches against alpha-synuclein in clinical trials to slow Parkinson’s progression. The positive results from this Alzheimer’s study are a boost that this therapeutic strategy shows real promise.

This excitement comes with a caveat, though. Biogen has a biomarker tool to measure the impact of its drug; Alzheimer’s researchers can measure amyloid load in the brain through imaging capabilities. We don’t have such a tool for Parkinson’s research yet.

Our senior vice president of research programs Mark Frasier, PhD, is at the International Conference on Alzheimer's and Parkinson's Diseases and Related Neurological Disorders in France, where Biogen shared its study results.

“I was at the presentation, and it was definitely impressive — both the changes on the biomarker scan but also the slowing of clinical progression. My takeaway from this entire meeting is how much we need better biomarkers of Parkinson’s disease,” he wrote in an email.

The Michael J. Fox Foundation is working urgently to validate Parkinson’s biomarkers. We’ve assembled a team to develop the technology to image the alpha-synuclein protein in the brain. And the MJFF-led Parkinson’s Progression Markers Initiative study is working toward measures of alpha-synuclein in blood or spinal fluid. Research toward these vital research tools is a top priority for the Foundation.

Learn more about PPMI and how biomarkers would speed testing of antibodies and other therapeutic approaches to slow Parkinson’s disease.

https://www.michaeljfox.org/foundation/news-detail.php?alzheimer-drug-shows-promise-in-slowing-disease&utm_source=social&utm_medium=facebook&utm_content=researchnews&utm_campaign=alzheimers-drug&s_src=researchnews&s_subsrc=alzheimers-drug#prclt-rvl1LfK9

New treatment could lead to a cure for Parkinson's disease

 Last updated: Thursday 26 March 2015 at 3am PST 15 Like12

Parkinson's disease, which took world fame after being diagnosed in various personalities such as actor Michael J. Fox, the heavyweight champion Muhammad Ali and the painter Salvador Dalí, could be very close to a cure, thanks to a Mexican researcher which managed to eliminate its neurological effects with an immunosuppressant.

Responsible for the scientific finding is Gabriela Caraveo Piso, researcher at the Whitehead Institute for Biomedical Research in the United States, who discovered that the role of calcium as an intracellular messenger can become lethal to brain cells when in high concentration.

Neurological diseases called synucleinopathies, such as Parkinson's, are characterized by the aggregation of alpha-synuclein protein. This action triggers a series of events such as the rise in intracellular calcium leading to over-activation of the enzyme calcineuria. This in turn removes phosphates (intracellular communication paths) to alter their functions and kill cells.

Gabriela Caraveo, a biologist graduated from the National Autonomous University of Mexico (UNAM), sought to nip this problem, after performing a series of analyzes in yeast, worms, and neurons of mice, found that by reducing the levels of activation of calcineurin, without eliminating it completely, the cells survived.

By modifying the activation of calcineurin contact with NFAT protein is cut out, and the communication to actin cytoskeletal rearrangements is redirected, which is responsible for cell morphology, thereby reducing failure in the motor function in animal models of Parkinson said the Mexican, who works in the lab of Susan Lindquist in the city of Cambridge, Massachusetts

To achieve adequate toxicity reduction the drug tacrolimus was used, which is administered clinically in newly transplanted patients to prevent organ rejection by the immune system.

Because calcineurin is also highly expressed in brain, this immunosuppressant that can cross the blood brain barrier is able to reduce the activation of calcineurin in the brain reducing the toxic symptoms of the disease. But it is important to adjust the dosage, because too much of it completely eliminates the activation of calcineurin preventing stimulation of protective pathways like the cytoskeleton leading to cell death.

"The dosage of the drug, also called FK506, I propose is well below the level of the immunosuppressants, which allows my work to have immediate treatment of neurological diseases characterized by the aggregation of alpha-synuclein as therapeutic implications as the Parkinson's disease," explained the specialist in neurosciences.

In healthy people, cells achieve to regulate the amount of intracellular calcium, the problem is when there are neurological diseases such as Parkinson's disease, the element is accumulated, becomes toxic and kills many neurons including dopaminergic neurons, responsible for implementing the motor functions.

According to preclinical results with tacrolimus pathologies associated to Parkinson's disease decreased in rodent models. The next step is to start human trials to test its effectiveness and safety as an alternative treatment that could even act as a cure.

http://www.medicalnewstoday.com/releases/291476.php?tw