A method based on artificial intelligence allows to diagnose Alzheimer's or Parkinson's

February 16, 2017

Researchers from the UGR and UMA have designed a technique that aims to model high-level data abstractions to make computers learn to differentiate the brain of a healthy person from that of an ill person by extracting the affected regions

UNIVERSITY OF GRANADA

Alzheimer's disease, which currently affects more than 40 million people, is the most common neurodegenerative disease in elder people.

Alzheimer's disease, which currently affects more than 40 million people, is the most common neurodegenerative disease in elder people. Early diagnosis is crucial both to treat the disease and to help the development of new medicines, as it hasn't been possible to find a cure so far. 

The development of Alzheimer's has been proven to be closely linked to structural changes -related to the gray matter, responsible for processing information- and functional ones -related to the white matter, which connects the different regions of the brain through fibers- in the brain connectivity network, since a significant loss of fibers also causes functional alternations, such as memory loss. 

However, diagnosis remains a challenge in spite of the scientific advances made, and to date it hasn't been possible to determine how functional cerebral activity deteriorates the structural one and vice versa, which is a key element to better understand the development of this type of diseases.

In this regard, computer aided diagnosis (CAD) is an important tool since it helps physicians to understand multimedia content obtained in tests carried out in patients, which allows a simpler and more effective application of the treatment. One such procedure is medical imaging, which provides high resolution "live" information on the subject matter and allows the use of information related to the disease contained in the image. The BioSip research team, belonging to the University of Malaga, in collaboration with a group of researchers from the University of Granada, has been studying biomedical images and signals for years.

Researchers Andrés Ortiz, Jorge Munilla, Juan Górriz and Javier Ramírez (from the universities of Málaga and Granada) have recently published, in the renowned International Journal Of Neural Systems, a similar article called Ensembles of deep learning architectures for the early diagnosis of the Alzheimer's disease. Said study presents a method for the diagnosis of Alzheimer's by the fusion of functional and structural images based on the use of the deep learning technique.

This Artificial Intelligence (AI) technique aims to model high-level data abstractions in order to enable computers to differentiate the brain of a healthy person from that of an ill person, by automatically extracting the affected regions of interest. As the researchers explain, "the study uses deep learning techniques to calculate brain function predictors and magnetic resonance imaging to prevent Alzheimer's disease. To do this, we have used different neural networks with which to model each region of the brain to combine them afterwards".

The study explores the construction of classification methods based on the Deep Learning architectures applied to brain regions defined by the Automated Anatomical Labeling (AAL), a digital atlas of the human brain. To this end, images of the gray matter of each area of the brain have been divided according to the regions separated in different sectors by the AAL, which have been used to train deep learning neural networks specialized in the different regions of the brain. The knowledge acquired by said networks is subsequently combined by different fusion techniques presented in this paper.

Classification architecture

The result of this work is a powerful classification architecture that combines supervised and unsupervised learning to automatically extract the most relevant features of a set of images. The proposed method has been evaluated using a large database from the Alzheimer's Disease Neuroimaging Initiative (ADNI).

The results of this work, which has included patients with other cognitive deficits that can develop Alzheimer's within two years, show the potential of AI techniques to reveal patterns associated with the disease. The accuracy rates obtained for the diagnosis allow to take a great step in the knowledge of the neurodegenerative process involved in the development of the disease, besides being useful as a starting point for the development of more effective medical treatments.

On the other hand, the techniques developed may serve as a starting point for the improvement of accuracy in the diagnosis of other dementias such as Parkinson's disease.

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In addition, the methods developed are being used for the improvement of diagnosis and for researching the biological origin of learning disabilities, such as dyslexia, in a project funded by the Ministry of Economy and Competitiveness.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

https://www.eurekalert.org/pub_releases/2017-02/uog-amb021617.php

Researchers Use Plasma Profiling to Identify Biomarkers Linked with PD Prognosis

February 15, 2017

Metabolic plasma profiling of mildly affected patients with Parkinson's disease identified 15 biomarkers that strongly predicted disease progression up to two years later, according to a new study published online on February 8 in Neurology.

Previous efforts at identifying biomarkers have focused on PD pathology in the brain, but recent research indicates this scope may be too narrow, since proteins associated with PD, such as alpha-synuclein, have been shown to spread throughout the body. Researchers hypothesized that a metabolomic analysis, which measures "hundreds of low-molecular-weight compounds in biospecimens" may be able to identify biomarkers in plasma that can predict the progression of PD.

The findings yielded several biomarkers strongly capable of predicting PD progression, the study authors, led by Peter A. LeWitt, MD, director of the Parkinson's Disease and Movement Disorders Program at Henry Ford Hospital in West Bloomfield, MI,  and professor of neurology at Wayne State University School of Medicine, wrote. "Having biomarkers could provide insights into sub-types of PD and might be useful in assessing the effectiveness of neuroprotective treatments," Dr. LeWitt said in an interview about the study appearing in the March 2 issue of  Neurology Today.

For the study, researchers twice collected concentrated samples of plasma and cerebrospinal fluid (CSF) from 49 mildly affected patients with PD: once at baseline and once at a final assessment up to two years later. They used ultra-high-performance liquid chromatography to identify small-molecule plasma constituents in the samples. At baseline and final assessment, the researchers assessed the patients' disease progression using questions from the Unified Parkinson's Disease Rating Scale (UPDRS) parts 2 and 3, which comprise an assessment of daily living activities and motor skills.

The researchers identified 15 baseline plasma constituents with a high positive correlation to changes in parkinsonian severity (0.87 correlation coefficient, p=2.2e-16). However, the CSF samples showed little change between the baseline and final assessments and had minimal correlation with change in UPDRS scores.

The findings, the study authors concluded, "discern a biochemical profile linked to PD progression," although they do not clarify whether the observed markers are manifestations of the disease process. They also imply "several new directions for investigation of PD pathogenesis." For example, one of the biomarkers identified, serine, has neurochemical properties that may pertain to PD and is involved in the synthesis of an antioxidant that is diminished in PD.​

Look for expanded coverage of the study in the March 3 issue of Neurology Today.

LINK UP FOR MORE INFORMATION:

• LeWitt PA, Li J, Lu M, et al. Metabolic biomarkers as strong correlates of Parkinson disease progression. Neurology 2017; Epub 2017 Feb 8.

http://journals.lww.com/neurotodayonline/blog/breakingnews/pages/post.aspx?PostID=603

The NeuroMedical Center in Baton Rouge Helps Advance New Parkinson’s Treatment

February 16, 2017

NMC Movement Disorder Specialists report success in late-phase clinical trial for new inhalable drug for “off” periods

BATON ROUGE, LA, 

Movement disorder specialists at The NeuroMedical Center in Baton Rouge, Louisiana are pleased to announce their involvement in advancing a potential break-through treatment for Parkinson’s disease. A late-phase clinical trial investigating Acorda Therapeutic’s inhalable formulation of levodopa (L-dopa) showed statistically significant improvement in motor function in people with Parkinson’s disease experiencing “Off” periods. The results from the Phase 3 CVT-301-004 clinical trial performed at The NeuroMedical Center and other sites across the country are so promising, Acorda intends to soon file for permission to begin marketing the new drug in the U.S.

CVT-301 is being developed as a self-administered, inhaled levodopa therapy for the treatment of symptoms of “Off” periods in people with Parkinson’s disease taking an oral carbidopa/L-dopa regimen. “Off” periods refer to stages experienced by patients with Parkinson’s disease when medication is not working well, and symptoms are exacerbated. CVT-301 aims to deliver a precise dose of a dry powder formulation of L-dopa to the lung to offer faster symptom control than tablets.

Phase 3 enrolled a total of 339 participants who were on a stable regimen of oral carbidopa/levodopa and randomized them to receive one of two doses of CVT-301 or a placebo. Subjects self-delivered the inhaled formulation up to five times a day for 12 weeks. At the completion of the trial, CVT-301 showed statistically significant improvement of motor function compared to the placebo.

The NeuroMedical Center’s Dr. Rebecca E. Whiddon, served as the trial’s principal investigator. Fellow Movement Disorder Specialists including The NeuroMedical Center’s Chief of Neurology, Dr. Gerald J. Calegan, and Dr. Glenn Kidder, served as sub-investigators for the study.

“We are greatly encouraged by the efficacy of this trial conducted at The NeuroMedical Center and hope that our involvement will advance this potentially important therapy for patients everywhere who are suffering with Parkinson’s,” said Dr. Whiddon. “Off periods can be very disruptive and uncomfortable for people with Parkinson’s, and we look forward to the future possibility of offering our patients another important treatment option to further manage symptoms of this extremely challenging disease.”

About Parkinson’s Disease and OFF Periods

Parkinson’s is a progressive neurodegenerative disorder resulting from the gradual loss of certain neurons responsible for producing dopamine. It causes a range of symptoms including impaired movement, muscle stiffness and tremors. “Off” periods refer to the phenomenon of Parkinson’s medications wearing off before the next dose of medication is taken. When this occurs, patients typically have to take medications more often; some patients have to take medications every 2-3 hours to prevent the medications from wearing off. “Off” periods typically begin several years after diagnosis/treatment of PD. “Off” periods are usually very uncomfortable, and patients often experience some or all of the following symptoms during an “Off” period – tremors, stiffness, painful spasms, shuffling gait, anxiety, panic, trouble thinking, dizziness, major increase or decrease in blood pressure, hot or cold sweats, as well as other symptoms.

Approximately one million people in the U.S. are diagnosed with Parkinson’s disease. “Off” periods are experienced by approximately 350,000 Americans, or one-third of patients with Parkinson’s disease.

About Acorda Therapeutics

Founded in 1995, Acorda Therapeutics is a biotechnology company focused on developing therapies that restore function and improve the lives of people with neurological disorders.

About The NeuroMedical Center

The NeuroMedical Center in Baton Rouge, Louisiana has led the South in expert neurological care since 1978. It is home to the region’s largest team of board certified and fellowship trained neurologists who work in detailed collaboration with other neurological specialists including neurosurgeons, physical medicine and rehabilitation (PM&R) specialists, pain medicine physicians, neuropsychologists, and neuroradiologists to deliver the most innovative, patient-centered care available for you and your loved ones. Our Neurology department and Clinical Research department is located on the 4th floor of The NeuroMedical Center Clinic located at 10101 Park Rowe Avenue. For appointments, please call (225) 768-2050.

http://www.satprnews.com/2017/02/16/the-neuromedical-center-in-baton-rouge-helps-advance-new-parkinsons-treatment/

Finally: Parkinson disease: Spanish research team found two major keys of the neuroprotection and natural increase of dopamine

February 15, 2017

Ramón Cacabelos, a world known expert for neurodegenerative disorders and genomic medicine, and his team have completed preclinical and clinical studies with a nutraceutical called AtreMorine. The exceptional results shows that AtreMorine protects selectively dopaminergic neurons and significantly increases naturally the dopamine level in the organism and without any reverse effects. 

Parkinson’s disease, with known symptoms as tremors, stiffness, slowness of movements, depression and other , is mainly due to the progressive degeneration of dopaminergic neurons. These dopaminergic neurons are quite rare in the brain and they die gradually.

An estimated loss of 5 to 10% of these neurons degenerate per decade in everybody’s brain and this process starts more or less at the age of 20. This degeneration occurs even more rapidly in persons affected by Parkinson’s disease and once the loss of these neurons reaches the critical 60-80% barrier, all known symptoms of this disease appear.

To produce dopamine, the body needs its precursor L-dopa. If L-dopa is given to the organism, it will transform it into dopamine. If the body can not produce enough dopamine through its dopaminergic neurons because too many of them died, then we give the synthetic drug L-dopa producing good results for an average of 3 to 10 years. But as we know, unfortunately, despite the very interesting and confirmed results on the symptoms, especially in the early phases, these conventional medical drugs are not able to cure and the destruction of the remaining dopaminergic neurons continues.

Professor Ramon Cacabelos and his team studied and developed during the last seven years this exceptional bioproduct which has significant performances over disorders due to the lack of dopamine which is the case of Parkinson’s disease.

This study was recently published in the “Journal of Genomic Medicine and Pharmacogenomics Scitcentral” with all references to the pre-clinical and clinical results of this nutraceutical whose scientific name is E-PodoFavalin-15999, distributed under the name AtreMorine.

The participants in this clinical study were divided into two groups: on one side the Parkinson patients being already in long term treatment with classical antiparkinsonian drugs and on the other side Parkinson’s patients never being in a medical treatment against Parkinson.

The first remark was that 100% of patients without antiparkinson treatment had dramatic hypodopaminergic levels, with dopamine plasma below 20 pg / mL. This is far to less for the body and this make it evident that it is important to take medical treatments in the case of Parkinson’s disease.

Respecting the other scientific results of this study, they were numerous, very promising and encouraging in both groups of patients giving significant solutions for Parkinson’s patients:

The scientific study reveals, that the first beneficial effect of AtreMorine is the selective protection of dopaminergic neurons, that means:

“so far, no remedy allowed to stop or decrease significantly the loss of dopaminergic neurons, but thanks to AtreMorine that is possible now.”

The second most important beneficial effect of AtreMorine for Parkinson patients, revealed in the study, is its ability to increase significantly levels of dopamine in the body thanks to the enormously rich content of natural L-DOPA (average concentration: 20mg/g). 

The scientific study indeed showed that:

“A single dose of 5-10 grams of AtreMorine increases dopamine levels in average range by 500% – 4000% in 30 minutes, and it’s effects remain up to 12 hours, improving in parallel the cardinal symptoms of Parkinson’s disease: tremor, bradykinesia and rigidity.”

The nutraceutical is made out of 100% natural plant extracts with a patented extraction method that protects the active principals. Another important factor the study showed, was the fact that the nutraceutical was tolerated by 100% of patients without any adverse effects.

AtreMorine has also shown other beneficial effects with a powerful regulation the noradrenaline and the hormones of the pituitary gland, such as prolactin and growth hormone which takes part in the control of supra-hypothalamic dopaminergic neurotransmission as mentioned in the study.

The noradrenaline as as well as the dopamine are very important in regulation of the mood of the persons. Many studies show that sadness and depression are regular phenomenon observed in almost 30% of patients with parkinson.

The study suggests that AtreMorine can contribute to:

• Reduce the phenomenon “wearing off” or “end-of-dose deterioration” (observed essentially in the intermediate and advanced phases).
• Help to improve the therapeutic effect of conventional antiParkinson drugs and delay the loss of long term response (from the initial to the advanced phase).
• Reduce at the same time the short term and long term adverse effects and long duration (from the initial to the advanced phase).

The study reveals precisely that co-administration of nutraceutical AtreMorine with antiparkinsonian drugs, allows a reduction of the conventional medicine dose between 25 to 50%, with clinical benefits and significant reduction of short and long term adverse of these drugs. Consequently, patients could use antiparkinsonian drugs over a much longer period. 

This is how this nutraceutical showed its utility in all stages of Parkinson’s disease (initial, intermediate and advanced stages). It could also be an option particularly for patients with serious adverse reactions and who can not take antiparkinson drugs or those having greater tolerance to natural products.

The promising results of this study suggests that AtreMorine contribute to significantly improve the lives of thousands of persons and their families nowadays. In addition to this, Atremorine could not not only help persons already suffering with parkinson’s disease and who need urgent help right now, but also help to prevent degeneration by persons exposed to a high level of pesticides for example, or those with medical family records for Parkinson’s disease.

Atremorine is situated first of all as a complement to the anti-parkinsonian drugs with their beneficial effects over the symptoms.

Other scientific articles on the nutraceutical are published on the websites of the following journals: “Journal of Nutrition & Food Sciences”; “Clinical & Medical Biochemistry“;  “Predictive, Preventive and personalized Medicine & Molecular  Diagnostics” ; “Journal of Exploratory Research in Pharmacology”

The nutraceutical AtreMorine is for the moment only available only on official websites of the product.

https://livebetterparkinsons.com/finally-parkinson-disease-spanish-research-team-found-two-major-keys-of-the-neuroprotection-and-natural-increase-of-dopamine/


ALWAYS SPEAK TO YOUR DOCTOR BEFORE TRYING ANY DRUGS.

FoxFeed Blog: First Trial Begins Testing Drug in People with GBA Mutation

Maggie McGuire Kuhl
February 14, 2017

Sanofi Genzyme has started a clinical trial for a drug targeting cellular dysfunction seen in people with Parkinson's disease (PD) and a GBA mutation. This study is a major step for PD research as it is the first drug trial where one's genetic information determines eligibility and is testing a potential therapy to slow or stop disease progression.

"I think of this as precision medicine for Parkinson's," Pablo Sardi, PharmD, PhD, research and development director in neuroscience at Sanofi wrote to news and information site Alzforum. Dr. Sardi announced the study at the Society for Neuroscience conference in November.

Precision or personalized medicine means developing and testing therapies based on one's molecular profile rather than on a clinical diagnosis. As we learn more about genetic mutations that may cause Parkinson's disease and the cellular dysfunction associated with those mutations, the research field moves to create more targeted treatments that may have greater success.

"We will only get to true cures if we can move away from historical clinical disease definitions, based purely on symptoms, to one more nuanced and linked to underlying biology, genetics and pathology," wrote MJFF leaders in a recent editorial in the journal Personalized Medicine.

Listen to a podcast or watch a webinar on Parkinson's personalized medicine.

Targeting Dysfunction Seen with GBA Mutations

GBA mutations cause dysfunction in the glucocerebrosidase (GCase) protein, which can lead to build-up of the protein alpha-synuclein. Clumps of alpha-synuclein (Lewy bodies) are seen in brain cells of everyone with Parkinson's disease, and scientists believe Lewy bodies harm cells, causing symptoms and progression. Read more about the connection between GBA, GCase and PD.

The Sanofi trial is testing a drug (GZ/SAR402671) against a partner of GCase and alpha-synuclein. GCase normally breaks down fatty substances (lipids). Build-up of one lipid (glucosylceramide) -- due to a GBAmutation -- may lead to build-up of alpha-synuclein. The company is testing an inhibitor of glucosylceramide, which they believe may prevent alpha-synuclein clumping and protect brain cells.

Laboratory tests showed pre-clinical PD models with a GBA mutation treated with a similar compound had fewer alpha-synuclein clumps and did better on memory tests than similar models not given the drug.

Recruiting Participants with Parkinson's and Known GBA Mutation

The Phase II trial recently began enrolling people with PD and a GBA mutation and aims to enroll 230 people across 50 international sites. The company expects to complete the trial by 2022. While currently one must know if they carry the mutation to enter the study, Sanofi Genzyme plans to offer genetic testing for individuals who meet other screening criteria in the future.

Who carries GBA mutations? These variants are more common in people of Ashkenazi Jewish descent and in people with Gaucher disease or a relative with Gaucher. This disorder, where fatty substances build up and cause enlarged organs, is also caused by a GBA mutation. It's important to note while GBA mutations are common, their chance of leading to Parkinson's disease is low.

In studies such as the MJFF-led Parkinson's Progression Markers Initiative (PPMI), researchers are observing people with GBA mutations (with and without PD) to understand more about what may lead some to develop the disease while others do not. [Sanofi Genzyme is one of 19 PPMI industry partners.]

PPMI is recruiting people of Ashkenazi Jewish descent with PD, Gaucher or a relative with either disease for genetic screening and counseling to see if they're eligible to participate in the study, a large-scale effort to learn more about PD variability and progression. Take a screening survey to see if you're eligible.

Have questions about where else to access genetic testing and counseling? Discuss your options with your movement disorder specialist.

Broadening the Reach of This Therapy beyond PD and GBA

What if you don't have the GBA mutation? While this specific trial doesn't apply to you, the knowledge we gain from it, and other studies, may. Studying genetic connections in PD gives a greater understanding of disease mechanisms and leads toward therapies that could potentially be applicable to the broader Parkinson's community, regardless of genetic status.

GZ/SAR402671 is currently in Phase II trials for Gaucher disease type 3 and Fabry disease, and other companies are also working on drugs to correct the dysfunction seen in PD and associated with GBAmutations.

The Sanofi trial is just starting, so not many sites are activated yet. Register with our online tool Fox Trial Finder to be matched with recruiting studies looking for volunteers like you and monitor the trial's page for updates. We'll share more on our blog and social channels as this study continues.

https://www.michaeljfox.org/foundation/news-detail.php?first-trial-begins-testing-drug-in-people-with-gba-mutation

Axovant Publicizes Preliminary Results of Phase 2 Trial of Nelotanserin

 FEBRUARY 15, 2017  BY PATRICIA INACIO, PHD IN NEWS

Axovant Sciences has announced the preliminary results of a Phase 2 clinical trial testing the investigational oral drug therapy nelotanserin in patients with either dementia caused by Lewy bodies (DLB), or Parkinson’s disease dementia (PDD).

Nelotanserin is an investigational drug candidate that binds to a receptor of the central nervous system, called 5HT2A receptor, which has been implicated in mental disorders and is associated with neuropsychiatric disturbances, including visual hallucinations. Nelotanserin binds to the 5HT2A receptor, but prevents the receptor from activating its response. Researchers call this type of drug an inverse agonist.

The study is an ongoing Phase 2 trial where enrolled patients scored 18 or higher on Mini Mental State Examination (MMSE), a questionnaire extensively used in clinical and research settings to assess the level of patients’ cognitive impairment.

Enrolled participants were assigned randomly to a regimen that includes first a placebo followed by nelotanserin, or nelotanserin followed by placebo. Treatments went on for four weeks with either regimen, followed by a “washout” period (no therapy) again of four weeks. During treatment, participants are treated with 40 mg nelotanserin (two weeks) and then with 80 mg nelotanserin (two weeks).

The trial’s primary outcome goal included the drug’s safety and its effects on the Unified Parkinson’s Disease Rating Scale (UPDRS) Parts II + III, a scoring system widely used for the clinical evaluation of Parkinson’s disease. UPDRS Parts II + III was measured at two time-points, at baseline and at the end of each four-week treatment period.

Secondary outcome measures included alterations to the severity and frequency of visual hallucinations, as determined by the Scale for the Assessment of Positive Symptoms (SAPS).

The preliminary results showed a significant improvement in mean change from baseline in the UPDRS Parts II + III in participants treated with nelotanserin relative to placebo. Moreover, no drug-related serious adverse events were reported, as well as any case of discontinuation of the medication due to side effects. The assessed secondary endpoints showed no statistical significant differences between nelotanserin and placebo.

These preliminary results have prompted Axovant Sciences to continue to investigate nelotanserin effects, and for that reason they are expanding patient recruitment to confirm the initial benefits with nelotanserin treatment.

A Phase 3 registration program is due to begin in the second half of this year.

“I am intrigued by the benefits observed on the UPDRS in this study,” said James Leverenz, MD, chairman of the Scientific Advisory Council of the Lewy Body Dementia Association, in a press release. Leverenz also is director of the Cleveland Lou Ruvo Center for Brain Health at the Cleveland Clinic. “If a single drug could simultaneously address the motor and neuropsychiatric symptoms of Lewy body dementia, which the published literature suggests may be the case for 5HT2A antagonists, it would represent a unique and important advance for the treatment of this condition. I look forward to reviewing the full dataset later this year,” Leverenz said.

“We are pleased with the preliminary results of this small pilot study which supports our belief that nelotanserin could be a promising investigational drug candidate for patients suffering from Lewy body dementia,” added Lawrence Friedhoff, MD, PhD, and chief development officer of Axovant Sciences. “We plan to discuss with FDA and other regulators the parameters of a potential Phase 3 registration program while we await results from the full cohort of patients in this study. We will carefully examine whether the UPDRS treatment benefit observed in this interim analysis will be maintained in the final analysis when the remaining patients complete this study.”

https://parkinsonsnewstoday.com/2017/02/15/axovant-phase-2-trial-preliminary-results-nelotanserin-parkinsons/

New Parkinson’s & Movement Disorders Program Launches

February 15, 2017

IRVINE, CA 

Silverado today announces an innovative program specifically designed to provide quality of life to people with Parkinson’s disease and other movement disorders. Available in Houston and Chicago, the specialized program was designed based on the latest Parkinson’s research combined with Silverado’s 20 years of experience serving people with movement disorders, which historically has affected about 15 percent of its residents

“Silverado’s ability to tailor programming for people with movement disorders will make a dramatic impact on lives as conditions such as Parkinson’s disease continue to affect a growing number of individuals,” shares Silverado President, CEO and Chairman Loren Shook. “Our communities combine world-class clinical care with social programs and a focus on brain health, resulting in the best clinical outcomes in our industry. This has created an optimal environment for serving people with movement disorders.”

The new program builds on Silverado’s Nexus program for people with early-stage memory impairment based on six areas of research showing that there may be ways to slow the progression of cognitive decline. In addition, the Parkinson’s & Movement Disorders Program includes physical, speech, and occupational therapies; support from a dedicated restorative aide and specially trained staff who have completed curriculum from the National Parkinson’s Foundation; medication management to ensure medication on time, which is critical to prevent motor fluctuations; Silverado’s award-winning fall reduction program; resident support groups led by masters-level social workers; and the concept of “dignity with risk”, a commitment to respecting each individual’s freedom of choice and autonomy.

The program is focused on the needs of those with Parkinson’s disease and other movement disorders, such as Progressive Supranuclear Palsy (PSP), Corticobasal Degeneration (CBD) and Multiple System Atrophy (MSA).

Silverado’s clinical team led development of the evidence-based program. In addition, they leveraged the company’s long-term research affiliations with top universities, including Baylor College of Medicine and Rush University, resulting in the opportunity to collaborate in this new specialization. Furthermore, Silverado intends to expand the program into additional markets later this year.

Families and professionals interested in learning more about the program can call Silverado Orchard Park at 847-583-9800 in Chicago or Silverado Cypresswood at 281-955-0880 in Houston. More information is also available at silverado.com/movementdisorders.

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About Silverado

Silverado was founded in 1996 with the goal of enriching the lives of those with memory loss by changing how the world cares for people with cognitive decline. Establishing this mindset as the foundation allows Silverado to operate in a way that provides clients, residents and patients with utmost dignity, respect and quality of life. Silverado has grown to become a nationally recognized provider of home care, memory care assisted living and hospice services. With 52 locations, the company delivers world-class care across Arizona, California, Illinois, Texas, Utah, Washington and Wisconsin. Learn more at silveradocare.com or call (866) 522-8125.

MEDIA CONTACT:

David Gill

(714) 624-2550

dgill(at)silveradocare(dot)com

http://www.satprnews.com/2017/02/15/new-parkinsons-movement-disorders-program-launches-2/

Alzheimer's May Be Linked to Defective Brain Cells Spreading Disease

February 15, 2017

Rutgers scientists say neurodegenerative diseases like Alzheimer’s and Parkinson’s may be linked to defective brain cells disposing toxic proteins that make neighboring cells sick.

In a study published in Nature, Monica Driscoll, professor of molecular biology and biochemistry, School of Arts and Sciences, and her team, found that while healthy neurons should be able to sort out and rid brain cells of toxic proteins and damaged cell structures without causing problems, laboratory findings indicate that it does not always occur.

These findings, Driscoll said, could have major implications for neurological disease in humans and could possibly be the way that disease can spread in the brain.

“Normally the process of throwing out this trash would be a good thing,” said Driscoll. “But we think with neurodegenerative diseases like Alzheimer’s and Parkinson’s there might be a mismanagement of this very important process that is supposed to protect neurons but, instead, is doing harm to neighbor cells.”

Driscoll said scientists have understood how the process of eliminating toxic cellular substances works internally within the cell, comparing it to a garbage disposal getting rid of waste, but they did not know how cells released the garbage externally.

“What we found out could be compared to a person collecting trash and putting it outside for garbage day,” said Driscoll. “They actively select and sort the trash from the good stuff, but if it’s not picked up, the garbage can cause real problems.”

Working with the transparent roundworm, known as the C. elegans, which are similar in molecular form, function and genetics to those of humans, Driscoll and her team discovered that the worms – which have a lifespan of about three weeks -- had an external garbage removal mechanism and were disposing these toxic proteins outside the cell as well.

Ilija Melentijevic, a graduate student in Driscoll’s laboratory and the lead author of the study, realized what was occurring when he observed a small cloud-like, bright blob forming outside of the cell in some of the worms. Over two years, he counted and monitored their production and degradation in single still images until finally he caught one in mid-formation.

“They were very dynamic,” said Melentijevic, an undergraduate student at the time who spent three nights in the lab taking photos of the process viewed through a microscope every 15 minutes. "You couldn't see them often, and when they did occur, they were gone the next day."

Research using roundworms has provided scientists with important information on aging, which would be difficult to conduct in people and other organisms that have long life spans.

In the newly published study, the Rutgers team found that roundworms engineered to produce human disease proteins associated with Huntington’s disease and Alzheimer’s, threw out more trash consisting of these neurodegenerative toxic materials. While neighboring cells degraded some of the material, more distant cells scavenged other portions of the diseased proteins.

“These findings are significant,” said Driscoll. “The work in the little worm may open the door to much needed new approaches to addressing neurodegeneration and diseases like Alzheimer's and Parkinson's."

https://www.laboratoryequipment.com/news/2017/02/alzheimers-may-be-linked-defective-brain-cells-spreading-disease-0

Blood test as effective as spinal fluid test to distinguish between Parkinson’s and comparable diseases

February 15, 2017

Typically, doctors rely on a spinal fluid test to differentiate between patients with Parkinson’s disease and those with an atypical parkinsonism disorder (APD). However, a blood test may be just as accurate when determining whether a patient’s symptoms are caused by Parkinson’s or an APD, according to a study published by the American Academy of Neurology.

Atypical parkinsonism disorders like multiple system atrophy, corticobasal degeneration, and progressive supranuclear palsy are often hard to diagnose, as their symptoms are similar to those of Parkinson’s disease. However, it is crucial to receive a proper diagnosis early for the best treatment, not to mention the fact that treatment methods differ between Parkinson’s and the ADPs. Because spinal fluid tests are invasive and painful, they are not as simple as a blood test, so diagnosing ADPs is more complicated.

However, study author Oskar Hansson found “that concentrations of a nerve protein in the blood can discriminate between these diseases as accurately as concentrations of that same protein in spinal fluid.”

The study looked at 504 people in three different study groups. Two groups, one in England and one in Sweden, were comprised of healthy people and people who have had Parkinson’s or APDs for four to six years. The third study group was full of people who had one of the diseases for three years or less. Hansson found that the blood test was as accurate as the spinal fluid test—it was able to diagnose if someone had an APD or Parkinson’s in both early-stage patients and those who had the condition for longer than four or more years.

In patients who had Parkinson’s, the protein levels were around 10 picograms per milliliter, whereas those with an APD had levels of 20 picograms or higher. Hansson believes that the “lower concentrations of the nerve protein in the blood of those with Parkinson’s may be due to less damage to nerve fibers, compared to those with atypical parkinsonism disorders.”

The new study will pave the way for more accurate diagnoses in patients suspected of having Parkinson’s or an APD. The APDs progress faster and have a higher mortality rate than Parkinson’s, so identifying them quickly is extremely important. One drawback of the nerve protein test is that it can only tell if a patient has Parkinson’s or an APD—it is unable to specify which APD the patient has. Thankfully, it is easier to differentiate between the different APDs based on other symptoms.

http://www.belmarrahealth.com/blood-test-effective-spinal-fluid-test-distinguish-parkinsons-comparable-diseases/

Research identifies cellular recycling process linked to beneficial effects of enduring mild stress

February 15, 2017

Brief heat shock reduces protein aggregation in a C. elegans model of Huntington's disease. Credit: Caroline Kumsta, Ph.D.

Biologists have known for decades that enduring a short period of mild stress makes simple organisms and human cells better able to survive additional stress later in life. Now, scientists at Sanford Burnham Prebys Medical Discovery Institute (SBP) have found that a cellular process called autophagy is critically involved in providing the benefits of temporary stress. The study, published today in Nature Communications, creates new avenues to pursue treatments for neurological disorders such as Huntington's disease.

Autophagy is a means of recycling cells' old, broken, or unneeded parts so that their components can be re-used to make new molecules or be burned for energy. The process had previously been linked to longevity, in no small part because of research led by Malene Hansen, Ph.D., associate professor at SBP and senior author of the study. The new results suggest that long life and stress resistance are connected at the cellular level.

"We used C. elegans—tiny roundworms used to study fundamental biology—to test the importance of autophagy in becoming stress resistant," says Caroline Kumsta, Ph.D., staff scientist in Hansen's lab and lead author of the study. "They're a great model system because they're transparent, so you can easily observe what goes on inside them, most of their genes and molecular signaling pathways have functional counterparts in humans, and they only live a few weeks, which greatly facilitate measuring their lifespans."

Kumsta and colleagues incubated worms at 36 °C, significantly above the temperature they are usually kept at in the laboratory, for one hour. After this short heat exposure—a mild form of stress that improves the organism's survival—autophagy rates increased throughout the worms' tissues. When they exposed these heat-primed worms to another, longer heat shock a few days later, worms that were deficient in autophagy failed to benefit from the initial mild heat shock, as observed in heat-primed worms with intact autophagy.

The researchers reasoned that a mild heat stress might also improve the worms' ability to handle another condition that worsens with age—buildup of aggregated proteins, which is stressful for cells. To test this hypothesis, Kumsta used worms that model Huntington's disease, a fatal inherited disorder caused by neuronal proteins that start to stick together into big clumps as patients age, leading to degeneration throughout the brain. Exposing worms that make similar sticky proteins in different tissues to a mild heat shock reduced the number of protein aggregates, suggesting that a limited amount of heat stress can reduce toxic protein aggregation.

Our finding that brief heat exposure helps alleviate protein aggregation is exciting because it could lead to new approaches to slow the advance of neurodegenerative diseases such as Huntington's," says Hansen. "The results may also be relevant to Alzheimer's and Parkinson's, which are similarly caused by clumping-prone proteins."

Caroline Kumsta, Ph.D. Credit: Sanford Burnham Prebys Medical Discovery Institute (SBP)

"This research raises many exciting questions," adds Hansen. "For example, how does induction of autophagy by a mild heat stress early on make cells better able to survive heat later—what's the cellular memory? There's a lot to follow up on."

"A lot of people ask us if this means they should start going to the sauna or do hot yoga," jokes Kumsta. "That may not be an entirely bad idea—epidemiological studies do indicate that frequent sauna use is associated with longer life. But we have a lot more research to do to figure out whether that has anything to do with the beneficial induction of autophagy by heat stress that we see in C. elegans."

Kumsta recently received a promotion from postdoc to staff scientist in recognition of her leadership of this study.

Journal reference: Nature Communications

Provided by: Sanford-Burnham Prebys Medical Discovery Institute

https://medicalxpress.com/news/2017-02-cellular-recycling-linked-beneficial-effects.html