Bern study sheds light on the brain mechanism of arousal

Published on December 22, 2015 

Scientists from Bern have discovered a mechanism which is responsible for the rapid arousal from sleep and anesthesia in the brain. The results of their study suggest new strategies for the medical treatment of sleep disorders and recovery of consciousness in vegetative states.

Chronic sleep perturbances affect 10-20% of the population of Switzerland and almost everyone experiences sleep problems at least once in a lifetime. Beside the quantity of sleep that is often affected in insomnia, clinical and experimental studies emphasize that the quality of sleep (e.g., depth of  your sleep) is equally important for a good night's sleep and a complete recovery of «body and mind» functions. «The consequences of sleep perturbations on life quality go far beyond daytime sleepiness and mood alteration. Cognitive impairment, hormonal imbalance and high susceptibility to cardiac or metabolic disorders are amongst some of the negative impacts frequently associated with subtle chronic sleep problems», says Prof. Antoine Adamantidis from the Department of Clinical Research of the University of Bern and Department of Neurology at the Bern University Hospital.

The quantity and the quality of sleep are now considered as an early marker of many neurological disorders including Alzheimer's disease, Parkinson's disease, and schizophrenia. Unfortunately, pharmaceutical strategies combined with improved life hygiene have limited effect. «Personalized medicine» strategies for the treatment of either insufficient sleep quality or quantity are missing.

Brain circuits for arousal and consciousness

Therefore, intensive experimental research is conducted to understand how brain circuits control sleep-wake cycle and consciousness - an enigma in modern Neurosciences and an exciting key mystery to resolve. Together with fellow researcher Carolina Gutierrez Herrera and colleagues from Germany, Adamantidis made a dual discovery: his team identified a new circuit in the brain of mice whose activation causes rapid wakefulness while its inhibition deepens sleep. The study was published in the scientific journal «Nature Neuroscience».

Mammalian sleep is classically divided in two phases, including non-rapid eye movement (NREM) sleep or «light» sleep, and REM (or paradoxical) sleep or «deep»/dreaming sleep. Key brain circuits for those two states have been identified.,However, the precise underlying mechanisms - such as the onset, maintenance and termination of sleep and dreaming - remain unknown.

Adamantidis and Gutierrez Herrera identified a new neural circuit between two brain regions called hypothalamus and thalamus, which have been associated with EEG (electroencephalogram) rhythms during sleep. The activation of this circuit signals the termination of light sleep: using a recent technology called optogenetics, the researchers made neurons from the hypothalamus controllable with millisecond-timescale light pulses and showed that their transient activation during light sleep induced rapid awakenings, while their chronic activation maintains prolonged wakefulness. In contrast, optogenetic silencing of this circuit stabilizes light sleep and increases its intensity. In a translational analogy, hyperactivity of this circuit may cause insomnia, while its hypo-activity could be responsible for hypersomnia, making it a new therapeutical target for sleep disorders.

Causing emergence from anesthesia and unconsciousness

Interestingly, the arousal power of this circuit is so strong that its activation precipitates emergence from anesthesia and the recovery of consciousness. «This is exciting discovery since therapeutical approaches to recover from a vegetative or minimally conscious state are quite limited», says Adamantidis. Non-selective deep brain electrical stimulation has been used with some success, however the underlying brain mechanisms remain unclear. In this study, Adamantidis, Gutierrez Herrera and collaborators nailed down a selective brain circuit important for the recovery of consciousness.

The dual findings of the Bernese researchers shine light on the brain mechanism of arousal and opens new door for tailored medical treatment of sleep perturbances, and provide a roadmap for arousing patients from a vegetative or minimally conscious state. However, Adamantidis emphasizes that «even though we made an important step forward now, it will take some time before novel therapeutical strategies will be designed based on our results».

Source:

http://www.unibe.ch
http://www.news-medical.net/news/20151222/Bern-study-sheds-light-on-the-brain-mechanism-of-arousal.aspx

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

Dec. 22, 2015

A drug that boosts activity in the brain's "garbage disposal" system can decrease levels of toxic proteins associated with Alzheimer's disease and other neurodegenerative disorders and improve cognition in mice, a new study by neuroscientists at Columbia University Medical Center (CUMC) has found. The study was published today in the online edition of Nature Medicine.

"We have shown for the first time that it's possible to use a drug to activate this disposal system in neurons and effectively slow down disease," said study leader Karen E. Duff, PhD, professor of pathology and cell biology (in psychiatry and in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain) at CUMC and at the New York State Psychiatric Institute. "This has the potential to open up new avenues of treatment for Alzheimer's and many other neurodegenerative diseases." The drug used was rolipram, which causes nausea and thus is not a good drug for use in humans, but similar drugs do not incur nausea as a side effect and could go into clinical trials very quickly,

To remain healthy, brain cells must continually clear out old, worn, or damaged proteins, a task performed by a small molecular cylinder called the proteasome. The proteasome acts as a kind of garbage disposal, grinding up the old proteins so they can be recycled into new ones. In neurodegenerative diseases, proteins tagged for destruction accumulate in the brain's neurons, suggesting that the cell's proteasomes are impaired.

Using a mouse model of neurodegeneration, the researchers first discovered that tau--a toxic protein that accumulates in Alzheimer's and other brain degenerative diseases--sticks to the proteasome and slows down the protein disposal process.

Administering rolipram activated the proteasome and restored protein disposal to normal levels. The drug also improved the memory of diseased mice to levels seen in healthy mice.

Rolipram has been tested before in mice and was shown to improve memory, but the mechanism for how this occurred was unclear. The new research shows that by inhibiting of the PDE-4 enzyme, rolipram produces a physical change in the proteasome that increases its activity.

"We still don't know exactly where the activation is happening, but what's new is that we can modify the proteasome to increase its activity. There could be many other ways to do this," said the study's first author, Natura Myeku, PhD, an associate research scientist in pathology and cell biology at CUMC.

Drugs that target proteasomes in this way should work for any disease caused by the accumulation of abnormal proteins, including Alzheimer's, Huntington's, Parkinson's and frontotemperoral dementia.

"Treatments that speed up these cell disposal mechanisms should, in theory, only degrade abnormal proteins. We don't need to know what the toxic form of the protein is," Dr Duff said. "In Alzheimer's disease, there are at least four different types: amyloid, tau, alpha-synuclein, and TDP43. A well-functioning proteasome can clear out everything at once."

"This exciting research from Dr. Duff's team advances our basic understanding of the proteasome system, provides a way to repair the system when it breaks, and alleviates symptoms of neurodegenerative disorders," said Rod Corriveau, PhD, program director at the National Institute of Health's National Institute of Neurological Disorders and Stroke, which provided funding for the study.

Source:

Columbia University Medical Center

http://www.news-medical.net/news/20151222/Drug-that-boosts-activity-in-the-brains-garbage-disposal-system-may-slow-Alzheimers-disease.aspx

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

Published on December 22, 2015 

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

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

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

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

Source:

Boston University Medical Center

http://www.news-medical.net/news/20151222/Benjamin-Wolozin-receives-24500000-award-in-Alzheimers-Disease-Drug-Discovery-Research.aspx

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

Published on December 18, 2015

A team of scientists at the University of Nebraska Medical Center (UNMC) and Longevity Biotech, Inc., has demonstrated that neuroprotection could be attained in preclinical models by a novel drug candidate that changes immune responses.

The results, published today in the Journal of Neuroscience, describe the prevention of nerve cell damage in a mouse model of Parkinson's disease. Notably, the drug protected nerve cells that produce dopamine, which is the chemical responsible for agility and movement that is lost in human disease.

"The results are exciting as they provide a bridge between the immune system and nerve cell protection in Parkinson's disease," said Scott Shandler, Ph.D., co-founder and CEO of Longevity Biotech.

"The idea was birthed nearly a decade ago when specific types of circulating blood cells called lymphocytes were found to damage the types of nerve cells responsible for disease," said Howard Gendelman, M.D., the Margaret R. Larson Professor and chair of the UNMC Department of Pharmacology and Experimental Neuroscience. "The new Longevity Biotech drug (LBT-3627) was able to change the function of these cells from killing the nerve cells to protecting them. This is especially significant for the Nebraska team, as the mechanism parallels closely the human trials nearing completion for Parkinson's patients."

LBT-3627 is similar to the naturally occurring vasoactive intestinal peptide (VIP), a well-established anti-inflammatory peptide with beneficial effects across a variety of disorders. VIP is rapidly degraded by the body and is unable to distinguish between its two naturally intended receptors (VPAC1 vs. VPAC2). These limitations have stymied prior translational success using VIP.

In contrast, LBT-3627 specifically targets VPAC2 and demonstrates impressive biological durability. In addition, LBT-3627 has the potential to be administered orally, Dr. Shandler said, which would further improve its clinical prospects and make it more accessible for people with Parkinson's disease.

Preclinical studies performed by the UNMC team demonstrated that LBT-3627 could achieve up to 80 percent protection of dopamine-producing nerve cells in a mouse model of Parkinson's disease. Furthermore, the immune transformation also affected primary scavenger cells called microglia cells that were found ultimately responsible for the neuroprotective activities observed that halted brain damage.

"The key finding in our study was that a specific white blood cell subset was produced as a consequence of LBT-3627 treatment and provided protection of dopamine producing nerve cells from being damaged," Dr. Gendelman said. "The neurotoxic immune reaction was halted and LBT-3627 was able to prevent disease."

"There are limited therapeutic strategies available to Parkinson's patients," said Marco Baptista, Ph.D., senior associate director of research programs at The Michael J. Fox Foundation for Parkinson's Research, which supported this work together with the National Institute of Neurological Disorders and Stroke and a generous gift from the Blumkin Foundation in Nebraska. "This approach shows one avenue to potentially protect the brain cells affected by Parkinson's disease and alter disease progression."

Dr. Shandler said Longevity Biotech is currently progressing LBT-3627 through preclinical development and hopes to begin a Phase I clinical trial in humans by 2017.

http://www.news-medical.net/news/20151218/Novel-drug-candidate-prevents-nerve-cell-damage-in-mouse-model-of-Parkinsons-disease.aspx

PARKINSON'S DISEASE GENE SUPPRESSES CANCER

Dec. 23, 2015

Melanoma incidence is higher in people affected by Parkinson's Disease but the genetic link shared by both diseases was unknown. The Parkin gene (PARK2) is often mutated in Parkinson's Disease and is consequently sometimes a genetic cause of Parkinson's Disease. However, PARK2 is also a tumor suppressor gene both of melanoma predisposition and progression. Melanoma is a form of skin cancer more common in Parkinson's Disease. For more information go to : http://www.skincancer.org/skin-cancer-information/melanoma

An in-depth analysis of the PARK2 (Parkin) gene showed that mutations were present far more often in Parkinson's Disease, making Parkinson's Disease nearly four times more likely. The formation of the Parkin gene occurs in melanocytes but not in most cells in which there is melanoma. The formation of the Parkin gene in melanoma cell lines resulted in a drastic reduction of cell proliferation. Inhibition of the Parkin gene in melanocytes stimulated their proliferation.

The results show an important role for the Parkin gene (PARK2), not only in Parkinson's Disease, but also as a tumor suppressor both in melanoma predisposition and progression, which could explain the association between Parkinson's Disease and melanoma.

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

Complete abstract : http://www.ncbi.nlm.nih.gov/pubmed/26683220

http://www.viartis.net/parkinsons.disease/news/151223.pdf mail@viartis.net

©2015 Viartis 

http://www.viartis.net/parkinsons.disease/news.htm

DRINKING BEER SLOWS DOWN ALZHEIMER’S AND PARKINSON’S DISEASE

POSTED BY: ADMIN | DECEMBER 22, 2015

Drinking beer could prevent the damage of the brain cells, says a research carried out by Jianguo Fang and his colleagues of Lanzhou University’s school of chemistry. Drinking liquor is not a much appreciated practice in the past but partying has become a part of life these days. While the goodness of the wine is well known, it’s time to know something more about beer.

Beer is not usually considered an evil for health when taken in reasonable quantity, but the goodness of beer is sure to amaze the beer lovers. A compound called xanthohumol present in the beer is observed to have anti-carcinogenic, anti-oxidation and cardiovascular-protection properties.

During brewing, an ingredient called hops is added to the beer that gives a bitter and tangy taste to it. Hops are the female flower of the hops plant known to have quite some medicinal values. Hops are the source of the compound xanthohumol present in the beer that renders goodness to the beer. These xanthohumol are observed to protect neuronal cells present in the brain and thereby slows down the development of brain disorders, reports Fangs and his team.

The oxidative damage to the neuronal cells is responsible for the development of brain diseases, according to the research, said Fang. Brain defects like Alzheimer’s disease, Parkinson’s disease and other neurodegenerative conditions could be prevented or slowed down by the preventing the oxidative damage to these neuronal cells.

Alzheimer’s disease is a type of dementia that causes interruption in memory, thinking and behaviour in a person’s regular life, whereas Parkinson’s disease is a chronic and progressive movement disorder due to the death of vital nerve cells or neurons. No cure has been found for these neurodegenerative diseases so far, and if this research is to be believed, then it is no wonder a joy to the beer brewers and beer lovers.

To report problems or to leave feedback about this article, e-mail: saranya@ibtimes.com.au

http://healthpassion.info/drinking-beer-slows-down-alzheimers-and-parkinsons-disease/

When Parkinson’s Disease Affects Mood

When people think of Parkinson’s disease, what comes to mind are the physical effects — the rigid muscles, the tremors, the difficulty with movement.

But Parkinson’s disease is a disorder of the brain and nervous system and, as such, also can have an effect on the patient’s emotional state. Mood changes can arise from biochemical changes wrought by the disease, but they may also be related to the medications used to counter Parkinson’s or be a natural reaction to the patient’s loss of control over his own body.

Caregivers of people with Parkinson’s disease need to understand these potential mood changes and be ready to adjust to them. There is a lot a caregiver can do to help, either by determining the source of the problem or by responding to the patient’s feelings with care, compassion, and thoughtfulness.

Emotional Responses to Parkinson’s Disease

Some of the emotional responses that have been associated with Parkinson’s disease include:

• Depression. Up to half of all Parkinson’s disease patients end up dealing with depression. It is so prevalent that some doctors believe depression may actually be a symptom of Parkinson’s, possibly rooted in the way the disease affects the brain.
• Denial. Many patients with Parkinson’s disease react to the initialdiagnosis by refusing to accept the reality of their situation. That denial could be accompanied by feelings of anger, fear, and anxiety.
• Fatigue. Parkinson’s disease can transform the simplest body movements — standing up, walking around — into draining experiences. Because of this, patients might end up becoming withdrawn and introverted, making them less interested in socializing with others.
• Anxiety. Doctors believe Parkinson’s patients experience feelings of anxiety for a couple of reasons. They become anxious when they think about the future and what the disease holds in store for them. Patients also have been shown to experience anxiety before they are ready to receive their next dose of medication, when some of their symptoms begin to resurface, or when they have an “off” period in which their symptoms re-emerge. Up to 40 percent of Parkinson’s patients may experience anxiety at some point.
• Apathy. About one in three patients with Parkinson’s disease experience feelings of apathy. They might find it hard to care about anything, or hard to get up and get things done.

Parkinson’s Disease Meds Can Change Moods

The medications people take for Parkinson’s disease can cause some emotional problems as well.

“Medications can cause some psychotic symptoms, some hallucinations and paranoia. Oftentimes it’s benign and not too upsetting, but other times it can become very uncomfortable,” said Linda Pituch, a patient services manager for the Parkinson’s Disease Foundation.Parkinson’s Disease: On the Lookout for Depression

Depression is the most common mood disorder linked to Parkinson’s disease, so caretakers need to keep an eye out for warning signs. These include:

• Being indifferent to activities the person once enjoyed
• Having a sharp decrease or increase in appetite
• Having trouble focusing attention or concentrating
• Making statements about feeling worthless, or showing a general lack of hope for the future
• Feeling constant sadness
• Having recurring thoughts of suicide or death

Pituch recommends bringing a depressed Parkinson’s disease patient to the doctor as soon as possible. “Determine if that person is getting help for their depression,” she said. “That’s very important. If they’re not getting help, it’s going to be a very difficult battle to win.”

Parkinson’s Disease: Helping With Mood Issues

Some of the ways that caregivers can help Parkinson’s disease patients with emotional problems or mood changes include:

• Therapy. Getting your loved one into psychotherapy can be an important step in dealing with anxiety, depression, or apathy. The therapist can help the patient understand their moods and what is causing them, and can teach that person how to better guide and control their emotions.
• Medication. Some Parkinson’s medications help with these mood problems; others make them worse. Parkinson’s medications and antidepressants can help improve feelings of depression, fatigue, or anxiety. On the other hand, some of these medications can bring on hallucinations or psychosis, so medication levels may need to be adjusted or a new Parkinson’s medication may need to be considered if effects like those occur.
• Socializing. Re-establishing a person’s ties to the outside world can do much to lift his spirits, Pituch said. “Get them out socializing, and support them when they feel uncomfortable,” she suggests. “Help them come up with ways of framing the situation when they’re having an embarrassing moment, like if there’s a bit of drool or some food on their shirt, by coming up with a quip to say when these things happen.”
• Reassurance. Caregivers can help tremendously just by maintaining a calm, loving, and reassuring manner, Pituch said. This is particularly true if the patient is having hallucinations or psychosis. “Caregivers should not debate that what they’re seeing is wrong or not true,” she says. Instead, “they want to say things like, ‘You’re okay, I’ve checked and everything’s okay. This could be a side effect of the medication.'”

Parkinson’s is a complicated disease. Read as much as you can about it. Beyond Everyday Health, two good places to start are the Michael J. Fox Foundation for Parkinson’s Research and the Parkinson’s Disease Foundation.

By Dennis Thompson

http://mymedclinic.info/?p=2952

Linking a genome-wide association study signal to a LRRK2 coding variant in Parkinson's disease

Dec. 21, 2015

Genome-wide association studies have identified several loci associated with Parkinson's disease (PD). Whole-exome sequencing detects rare coding variants, but their links with PD genome-wide association study loci are unknown. Our objective was to investigate whether nonsynonymous variants in LRRK2 can explain associations at the PD-associated locus tagged by rs1994090. We sequenced all coding exons of LRRK2 in 453 East Asian samples and evaluated linkage disequilibrium between each nonsynonymous variant and rs1994090. We then tested selected variants and haplotypes for association with PD in 13,581 East Asian samples. Of all the nonsynonymous variants, only p.Gly2385Arg was in moderate linkage disequilibrium with rs1994090 and was observed on haplotypes tagged by the rs1994090-C risk allele. Conditional analyses showed that associations at these 2 variants are not independent. LRRK2 p.Gly2385Arg can explain most if not all of the PD association at rs1994090 in East Asians, but other nonsynonymous variants are independent. © 2015 International Parkinson and Movement Disorder Society. © 2015 International Parkinson and Movement Disorder Society.

http://www.topix.com/health/parkinsons-disease/2015/12/linking-a-genome-wide-association-study-signal-to-a-lrrk2-coding-variant-in-parkinsons-disease

CANTABio and Gardedam Therapeutics complete Merger to Tackle Development of Novel Therapeutics for Alzheimer's and Parkinson's Disease

December 21, 2015

PALO ALTO, Calif., Dec. 21, 2015 (GLOBE NEWSWIRE) -- 

Cantabio Pharmaceuticals, Inc. ("Cantabio") (OTCQB:CTBO) is pleased to announce the completion of its reverse merger (the "Merger") with Gardedam Therapeutics, Inc. ("Gardedam"). The effective date of the Merger is December 18th, 2015.

Cantabio will have an exclusive focus on the discovery and development of Gardedam's drug pipeline for neurodegenerative diseases such as Parkinson’s disease (PD) and Alzheimer’s Disease (AD).

As part of a large and developing portfolio of therapeutic candidates, Cantabio will first progress its research into the DJ-1 protein, advancing small molecule pharmacological chaperones and engineered blood brain penetrant DJ-1 drug candidates into pre-clinical development for the treatment of Parkinson’s and Alzheimer’s diseases.

Having completed the Merger, Cantabio issued 15.5 million shares of its common stock to the holders of Gardedam common stock. Under the terms of the Merger, these shares will be restricted from trading for a period of one year from the closing of the Merger. After the close of the Merger a total of 27.25 million shares of common stock will be outstanding.

Gergely Toth, MBA, PhD, founder of Gardedam and CEO of Cantabio, said, “The Merger strengthens our financial position allowing us to accelerate our drug discovery and development of clinical candidates for Parkinson’s and Alzheimer’s disease.  With recent research establishing a genetic link between the DJ-1 protein and familial and sporadic PD, AD and other neurodegenerative diseases we are particularly focused on rapidly advancing into clinical trials our novel DJ-1 protein therapeutic candidates. These may protect from oxidative stress and protein misfolding, both processes that have been linked to the onset and progression of these diseases. In view of the lack of approved therapies for Parkinson’s and Alzheimer’s diseases, our pharmacological chaperone and CNS penetrant engineered protein drug discovery technologies provide potential for the development of disease modifying clinical candidates with novel mechanisms of action.”

“I am delighted that we have been able to form a strong executive team, all graduates of the Executive MBA program at the Judge Business School at the University of Cambridge, with extensive scientific and business experience. We have also appointed an exceptional scientific advisory board and aim to build Cantabio into one of the leading discovery driven biotechnology companies focusing on the development of therapies targeting these neurodegenerative diseases. We have a strategy that is also strongly focused on delivering returns for investors and we are very excited about taking the company forward.”

About Cantabio Pharmaceuticals Inc

Cantabio Pharmaceuticals Inc. is a preclinical stage biotechnology company focusing on commercializing novel therapies and the intellectual property generated from its research and development activities. Its primary focus is on therapeutic candidates for Parkinson’s disease (PD), Alzheimer’s disease (AD) and other related neurodegenerative diseases. Cantabio’s strategy combines therapeutic focus, target family biophysics, drug discovery technology and expertise into an innovative drug discovery approach and its current main focus is on identifying and developing small molecule pharmacological chaperones for clinical trials. In addition, the company is developing therapeutic proteins that can pass through the blood-brain barrier to supplement existing levels of proteins, which display loss of function during disease conditions.

Notice Regarding Forward Looking Statements

This press release includes certain "Forward-Looking Statements" within the meaning of section 21E of the Securities Exchange Act of 1934, as amended. All statements regarding potential results and future plans and objectives of Cantabio Pharmaceuticals, Inc. are forward-looking statements that involve various risks and uncertainties. There can be no assurance that such statements will prove to be accurate and actual results and future events could differ materially from those anticipated in such statements. Important factors that could cause actual results to differ materially from our expectations include, but are not limited to, those factors that are disclosed under the heading "Risk Factors" and elsewhere in our documents filed from time to time with the Securities and Exchange Commission. Other risk factors may include, but are not limited to, fluctuation in quarterly results, and increased competition in our operations, our ability to continue operations as scheduled, and our ability to protect the proprietary technology we use. Further, the company operates in an industry sector where securities values are highly volatile and may be influenced by economic and other factors beyond the company's control, such as announcements by competitors and service providers.

The contents of this press release are presented as a general overview of the company. It is intended only to contain general information regarding the company and its business and does not purport to provide complete disclosure or analysis of all matters, which may be relevant to a decision to make an investment, including all risk factors or similar considerations. Although the information is believed current as of the date herein, the information may be subject to change, amendment or supplementation, and the company does not expect, and assumes no obligation, to update or otherwise revise the information herein.

 http://ir.cantabio.com/press-releases/detail/7/cantabio-and-gardedam-therapeutics-complete-merger-

COO Dr. Thomas Sawyer

@cantabio.com


(844) 200-CTBO

Source: Cantabio Pharmaceuticals Inc.

Released December 21, 2015

10 Tips for a Healthy Winter with Parkinson’s Disease

FoxFeed Blog

Posted by  Nancy Ryerson, December 18, 2014

Whether you’re traveling for winter holidays or staying warm at home, the season can bring along plenty of fun with family and friends but some stressors, too. There are a few precautions people with Parkinson’s can take to ensure the holiday season and the rest of winter is as healthy as possible.

1. Keep a routine. Even if you’re on vacation or have family visiting, be sure to exercise, get enough sleep and take your medications at the same time as usual.
2. Avoid the temptation to overeat or drink at holiday parties. Indulge in a treat or two but stick to your usual diet as much as possible, Rachel Dolhun, MD, recommends. “This is especially pertinent with regard to combining protein and carbidopa/levodopa (Sinemet) — try to take medication 30 minutes before or 60 minutes after meals and save most protein (ham or turkey, for example) for later in the day,” says Dr. Dolhun.
3. Watch out for depressive symptoms. Depression is common in Parkinson’s disease, and the shorter days and colder weather may lead one to feel more blue. Talk to your doctor right away if you feel you might be depressed.
4. Be careful of slippery conditions and ice. Speaking of cold weather, ice and slippery conditions can be particularly hazardous if you’re having trouble with balance. Walk in cleared walkways as much as possible, wear shoes with non-slip tread rubber on the bottom and bring along a cane or walker. You can even try ski poles or walking sticks to help steady yourself if necessary.
5. Keep a winter emergency kit handy in your home. Be sure to include several emergency light sources like battery-operated lanterns or touch lights, as well as spare batteries. Navigating a dark home can be particularly dangerous with gait or balance difficulties.
6. Don’t isolate yourself. If you’ve recently been diagnosed or your symptoms have worsened since you last saw certain friends and family, it can be tempting to sit out of holiday gatherings. But, social activities can help lift your mood and help reduce stress. “Participate in social activities as you are able and comfortable doing,” says Dr. Dolhun. “Attend a Christmas concert, bake cookies with a friend or go on a walk with neighbors to view outdoor decorations.”
7. Give yourself a break. Don’t feel pressured to participate in every festive activity you’re invited to. Again, stick to your regular schedule as much as possible. When you do decide to partake, allow extra time to prepare for and travel to activities so you don’t feel rushed or stressed.
8. Take advantage of online shopping for gift buying and avoid the malls if they are anxiety-provoking or make symptoms worse. Shopping on Amazon? The Amazon Smile program automatically gives a small percentage of your purchase to your chosen charity, including the Foundation.
9. Be prepared when traveling.  Consider letting airport staff know that you have Parkinson's disease -- you may be able to board the flight early or get extra help from a flight attendant. Also, be sure to always keep your medication on your person, rather than in a checked bag. Our community shared more tips for travel back in July.
10. Expect a few questions about Parkinson’s disease. Consider printing out our resource guide to share with family and friends who are interested in learning more about the disease.

https://www.michaeljfox.org/foundation/news-detail.php?10-tips-for-healthy-winter-with-parkinson-disease&os_cid=fb-a30U0000000OVlA&s_src=MJFFfb&s_subsrc=winter_safety_12.11