Good Shepherd leases space from Penn State Health St. Joseph for 14-bed inpatient rehabilitation facility

March 22, 2018   By From Good Shepherd

Good Shepherd Rehabilitation Network is planning to open a 14-bed inpatient rehabilitation facility at Penn State Health St. Joseph Medical Center in Bern Township, Pennsylvania, pending approval from the Department of Health. The inpatient rehabilitation facility is expected to open in early Fall 2018.

The 12,000 square foot facility will be located in existing space on the Garden Level of St. Joseph’s main campus off of Route 183 in Bern Township.

“Patients who receive care at St. Joseph will benefit significantly from this partnership,” says John R. Morahan, CEO of Penn State Health St. Joseph. “As an acute-care hospital and an accredited stroke center and with growing neurosciences and orthopedic programs, we will be able to offer access to specialized post-acute care within our Bern Township hospital.”

“The clinical partnership will close the loop on a seamless acute care/rehab experience,” continues Morahan. “Coupling continuity of physician care with the nationally-renowned expertise of Good Shepherd will make quality acute and rehab care readily accessible in one convenient location. An internal transfer to rehab care would be an ideal scenario for fragile patients as they start on the road to recovery.”

Good Shepherd will provide inpatient rehabilitation for patients who have experienced stroke, brain injury, spinal cord injury, major-multi traumas, complex joint replacements, amputation and other physical and neurological conditions, such as Parkinson’s disease and multiple sclerosis.

Services will include neurorehabilitation, physical and occupational therapy, speech/language therapy, oncology and cardiac rehabilitation and neuro-psychological services. Highly specialized rehabilitative medical care will be provided by on-site physiatrists, staffed by the Good Shepherd Physician Group, and a comprehensive rehabilitation care team representing various disciplines.

“Good Shepherd Rehabilitation Network is a nationally recognized rehabilitation leader and an international destination for recovery,” says John Kristel, President & CEO, Good Shepherd Rehabilitation Network. “We look forward to partnering with Penn State Health St. Joseph as well as the remarkable physicians and health-care providers in the greater Reading region to make access to world-class rehabilitative care more convenient for patients and families.”

Good Shepherd’s Bern Township inpatient rehabilitation facility will operate independently from Penn State Health St. Joseph, as a licensed service of Good Shepherd Rehabilitation Network. The Network expects to hire approximately 35 employees to staff the facility. St. Joseph’s will provide certain contracted services as part of the arrangement, including food and nutrition, housekeeping and ancillary services.

Good Shepherd Rehabilitation Hospital at Penn State Health St. Joseph will feature beautifully appointed private rooms, a leading-edge rehabilitation gym, a home-like suite to practice activities of daily living and easy access to outdoor space. The garden-level space being occupied by Good Shepherd had been shelled for future clinical services when St. Joseph opened in 2006.

http://www.berksmontnews.com/article/BM/20180322/NEWS/180329977

Man with Parkinson's Disease uses these props to spread awareness

March 22, 2018

CORNING, N.Y. (18 NEWS) - Bob Russell was diagnosed with Parkinson's disease in 2005. Parkinson's disease is a neurodegenerative disorder where the part of the brain that controls movement is affected.

He struggled with symptoms for the next six years on the job which involved sound, lights, and sets.

"I took my headsets off and put them on the deck and just put my head in my hands and said, 'I can't do this anymore.'" Russell said. "And that's it. I never went back to work."

The former stage manager loved the job so much, he thought he was going to work until he was 75, but eight surgeries later (two of those being brain surgeries because of the disorder), he says fate had different plans for him. 

The Corning native who now lives in Niagara County takes up to eight different types of medication a day to control his symptoms. The pills are spanned out every two and a half hours, so he has alarm after alarm set on his phone. 

Despite the inconvenience, he uses his experience to spread awareness to local students with encouragement from his wife.

"I love my wife dearly," Russell said. "She's been my best caregiver."

In addition to a presentation explaining what Parkinson's is, Russell brings along props to demonstrate and gets a kick out of the students trying to complete the tasks. 

The first prop includes wearing one boot with a three-pound weight to exemplify abnormal walking or posture.

Another demonstration includes putting on winter gloves, then trying to open a pill bottle filled with tic tacs, and pouring out one color of each. 

Lastly, students put Marshmallows in their mouth and try to say the alphabet to demonstrate slurred speech.

"The humor is the best thing to have when you have a terminal illness with no cure," Russell said. "You have to laugh at yourself and call yourself Parkys and say you're feeling a little Parky today."

Russell does his presentations for free, but he's received donations for the Parkinson's Foundation totaling $800. 

To see video:
http://www.mytwintiers.com/news/local-news/man-with-parkinsons-disease-uses-these-props-to-spread-awareness/1070165057

http://www.mytwintiers.com/news/local-news/man-with-parkinsons-disease-uses-these-props-to-spread-awareness/1070165057

Deep Brain Stimulation for Parkinson’s Disease: The Past and What the Future Holds

MARCH 23, 2018  BY PATRICIA INACIO, PHD IN NEWS.

Despite being used for the past 30 years to treat chronic neurological diseases, including Parkinson’s disease (PD), deep brain stimulation (DBS) “remains a fascinating puzzle to scientists, physicians, and engineers,” the lead author of a new review study said.

Challenges the technique presents for both clinicians and engineers include the design of novel, more efficient DBS therapies, the existence of redundancy in clinical outcomes, and a high variability in patients’ responses to the therapy, according to the review, which summarizes what has been achieved so far and what lies ahead for deep brain stimulation.

The review “Systems approaches to optimizing deep brain stimulation therapies in Parkinson’s disease” appeared in the journal WIREs Systems Biology and Medicine.

Deep brain stimulation involves surgically implanting an electrode in the brain that is connected to an implanted pulse generator through subcutaneous wires. The pulse generator is programmed to deliver charge-balanced, voltage-controlled electric pulses.

Currently, deep brain stimulation is recommended to Parkinson’s disease patients in relatively advanced stages of the disease, who are still responsive to anti-PD medications, but have developed medication-induced dyskinesia — in which patients experience involuntary, jerky movements.

The therapy helps improve dyskinesia and other motor complications, and is linked to a more efficient and prolonged management of disease symptoms and a lower usage of anti-PD medications (up to 50 percent).

“Although effective and generally safe, DBS [deep brain stimulation] remains a fascinating puzzle to scientists, physicians, and engineers,” lead author Dr. Sabato Santaniello, of the University of Connecticut, said in a press release. “The therapeutic mechanisms of DBS, in fact, are still elusive and the current, semi-permanent stimulation protocols have often motivated the investigation of ways to make DBS less invasive and more efficient.”

“The set of therapeutic DBS programs is overall larger than initially hypothesized. New tools and methods are therefore necessary to search this set and to systematically identify the most adequate DBS program for each patient,” the authors write in their review. “These solutions are still in their early stages and need to translate from preclinical testing phases to clinical trials.”

Developing more efficient deep brain stimulation therapies has proven challenging. The relatively poor understanding of the cellular mechanisms underlying deep brain stimulation therapeutic effects has impaired its progression.

In the review, the authors gather current data which suggests that novel, low-power deep brain stimulation solutions can be devised, preserving the clinical benefits of current DBS therapies while addressing its major limitations, such as inefficient battery consumption, the need for lengthy manual programming, and the widespread influence on nearby cognitive loops with possible adverse side effects.

There is currently little information on how variations in the different deep brain stimulation programs may lead to potential different outcomes.

There is also a high variability in patients’ responses to deep brain stimulation, which requires careful adjustments to the electric stimulation. Networks involving brain structures are made up of interconnected large groups of nerve cells where information may be corrupted and communicated with delays.

The technique also influences brain dynamics in a nontrivial way, as it changes the extracellular environment in surrounding structures, which in turn can affect the activity of each nerve cell.

https://parkinsonsnewstoday.com/2018/03/23/deep-brain-stimulation-for-parkinsons-disease-remains-fascinating-puzzle/

New PET Tracer with Potential to Diagnose Parkinson’s to Be Tested in First-in-Human Study

MARCH 23, 2018 BY JOSE MARQUES LOPES, PHD 

An innovative Positron Emission Tomography (PET) tracer that has the potential to diagnose Parkinson’s disease will soon be tested in humans for the first time.

Led by Switzerland-based AC Immune, which developed the technology, the study is expected to begin in the second half of 2018. The company recently presented the data on its new product at the AAT-AD/PDTM Focus Meeting 2018 in Turin, Italy.

“We are excited about this significant step in our development of potentially the first ever PET tracer for earlier and more accurate diagnosis of Parkinson’s,” Andrea Pfeifer, CEO of AC Immune, said in a press release. “This important milestone underlines our vision to become a global leader in precision medicine of neurodegenerative diseases, leveraging our proprietary technology platform.”

The company used its Morphomer platform, designed to interact with misfolded and aggregated proteins, to develop the PET tracer, which is highly selective for alpha-synuclein, enabling an earlier and more accurate Parkinson’s diagnosis.

AC Immune’s technology is aimed at not only detecting alpha-synuclein in patients, but also monitoring the effects of treatments targeting protein clumps. The research program has been spotting small molecules selective for alpha-synuclein and suitable for development as PET tracers.

Upon entering the brain, the new imaging agent, called a PET tracer, binds to abnormal or misfolded alpha-synuclein. Its radioactive label enables the imaging device to detect bound alpha-synuclein, informing clinicians on the amount and distribution of pathological brain alpha-synuclein.

If successful, the new PET tracer would be the first alpha-synuclein tracer to receive regulatory approval for commercial distribution. Its specificity would be important not only for Parkinson’s patients, but also for other disorders characterized by aggregated alpha-synuclein, collectively called synucleinopathies.

AC Immune has been collaborating with Biogen on this program since April 2016. The companies will proceed with the development and seek clinical validation for the use of the PET tracer as an imaging biomarker for Parkinson’s.

The Michael J. Fox Foundation for Parkinson’s Research (MJFF) is supporting this project. “We are very pleased about this next important step in the development of an alpha-synuclein imaging agent,” Jamie Eberling, PhD, director of research programs at MJFF, said.

“Having a PET tracer to detect and track Parkinson’s disease would be transformative for Parkinson’s research and patient care,” she said.

https://parkinsonsnewstoday.com/2018/03/23/pet-tracer-parkinsons-ac-immune-first-in-human-study/

The gene causing new brain disorder

March 23, 2018, Hokkaido University

MRI analysis of a patient with PSP-like symptoms showed severe atrophy of the bilateral hippocampus, mesencephalic tegmentum, cerebellum, and brainstem. Credit: Yabe I. et al., Scientific Reports, January 16, 2018

Newly discovered gene mutations may help explain the cause of a disease that drastically impairs walking and thinking.

Mutations have been found in the bassoon (BSN) gene, which is involved with the central nervous system, in patients with symptoms similar to, but different from, a rare brain disorder called progressive supranuclear palsy(PSP).

PSP, a form of Parkinson's disease, is often difficult to diagnose because it can affect people in different ways. Serious problems often include difficulty with walking and balance in addition to a decline in cognitive abilities such as frontal lobe dysfunction.

A team of Japanese researchers investigated patients whose symptoms resembled not only PSP but also Alzheimer's disease. Despite similarities in the symptoms, detailed pathological analyses showed no resemblance to either disease, which prompted the team to further research the new disease's underlying mechanism.

They first analysed the genomes of a Japanese family with several members displaying PSP-like symptoms. They identified a mutation in the BSN gene only in family members with symptoms. These individuals did not have mutations in the 52 other genes associated with PSP and other neurological disorders such as Alzheimer's and Parkinson's. This was the first time BSN gene is associated with a neurological disorder.

Tau proteins accumulated in the brain of a patient with PSP-like symptoms. Credit: Yabe I. et al., Scientific Reports, January 16, 2018

The researchers also detected three other mutations in the BSN gene in four out of 41 other patients displaying sporadic, or non-familial, PSP-like symptoms. None of the BSN mutations were detected in a random sample of 100 healthy individuals, underscoring the strong involvement of BSN mutations in the disease.

An autopsy done on one of the family members with the BSN mutation showed an accumulation of a protein called tau in the brain, which is not seen in a normal brain. The researchers believe that the BSN mutation is involved in the tau accumulation, which could cause the development of PSP-like symptoms. An experiment introducing a mutated rat BSN gene to cultured cells also suggested that the mutation causes the accumulation of tau. Communication between nerve fibres could also be affected, as BSN protein play a role in it.

"This is a peculiar neurodegenerative disorder which involves mutations in the BSN gene and tau accumulation, but differs from any known disease, including dementia, Parkinson's, and even PSP," says Associate Professor Ichiro Yabe of Hokkaido University who led the study. "Patients with PSP-like symptoms and other neurodegenerative disorders should be analysed for BSN mutations to fine-tune their diagnoses."

More information: Ichiro Yabe et al. Mutations in bassoon in individuals with familial and sporadic progressive supranuclear palsy-like syndrome, Scientific Reports (2018). DOI: 10.1038/s41598-018-19198-0 

Journal reference: Scientific Reports

Provided by: Hokkaido University

https://medicalxpress.com/news/2018-03-gene-brain-disorder.html

Launch of Parkinson’s Singing Group in Forth Valley

March 22, 2018

A new Parkinson’s Singing Group will be available in the Forth Valley area from Monday, April 16 at Alva Academy in Clackmannanshire from 4.30pm-6pm. 

The group is open to anyone who is affected by Parkinson’s, including family members and carers. Chloe MacMillan, Parkinson’s UK area development manager, said: “Singing can help people improve speech and strengthen muscles. 

“There is a strong social aspect, and lots of people find singing makes them feel better, which is really helpful for people who have anxiety or depression.” 

To find out more about the singing group, contact cmacmillan@parkinsons.org.uk

https://www.falkirkherald.co.uk/news/health/launch-of-parkinson-s-singing-group-in-forth-valley-1-4710595

Domain Therapeutics receives $125m to assign its intellectual property

March 22, 2018

Domain Therapeutics to receive up to $125 million for assignment of its intellectual property covering the Foliglurax mGluR4 PAM series discovered by a French biotech

Domain Therapeutics is pleased to congratulate its partner company Prexton Therapeutics on its acquisition by H. Lundbeck. Prexton’s drug candidate, Foliglurax, is currently in clinical Phase II for symptomatic treatment of OFF-time and dyskinesia (involuntary muscle movements) in Parkinson’s disease.

The series of compounds, from which Foliglurax originated, was initially discovered by Domain Therapeutics, licensed to Prexton in 2013 and assigned as part of the acquisition by Lundbeck. 

Foliglurax itself was identified by Domain who worked closely with Prexton to advance the programme from discovery to development. This first-in-class molecule is the only metabotropic glutamate receptor 4 Positive Allosteric Modulator (mGluR4 PAM) to have reached the clinic.

As a Prexton shareholder and patent assignor, Domain will receive up to $125 million depending on the successful outcome of certain undisclosed milestones.

“This transaction, one of the more significant recent trade sales of a European private biotechnology company, validates Domain’s strategy of partnering the development of its drug candidates through asset-centric companies,” said Pascal Neuville, CEO of Domain Therapeutics.

“The team at Prexton was excellent in rapidly moving Foliglurax through preclinical and early clinical stages in order to make this promising treatment available to the Parkinson’s disease patient population.”

“Our fruitful partnership with Domain resulted in the selection of Foliglurax that we successfully developed through these early development stages,” said Francois Conquet, Founder and CEO of Prexton.

“This collaboration is an example of complementarity between partners to jointly develop a valuable asset for a major indication.”

Companies 

• Lundbeck
• Domain Therapeutics

https://www.manufacturingchemist.com/news/article_page/Domain_Therapeutics_receives_125m_to_assign_its_intellectual_property/141009

New Finding on Parkinson’s Gene Mutation Alters View of What Causes the Disease

March 22, 2018

Source: Manu5/Wikimedia

• Scientists report that the most common Parkinson's gene mutation may change how immune cells react to generic infections like colds, which in turn trigger the inflammatory reaction in the brain that causes Parkinson's. Their study (“Mutant LRRK2 Mediates Peripheral and Central Immune Responses Leading to Neurodegeneration In Vivo”), published in Brain, contradicts the long-held view that Parkinson's was a disease that starts in the brain, destroying motion centers and resulting in the tremors and loss of movement.

  “Missense mutations in the leucine rich repeat kinase 2 (LRRK2) gene result in late-onset Parkinson’s disease. The incomplete penetrance of LRRK2 mutations in humans and LRRK2 murine models of Parkinson’s disease suggests that the disease may result from a complex interplay of genetic predispositions and persistent exogenous insults. Since neuroinflammation is commonly associated with the pathogenesis of Parkinson’s disease, we examine a potential role of mutant LRRK2 in regulation of the immune response and inflammatory signaling in vivo. Here, we show that mice overexpressing human pathogenic LRRK2 mutations, but not wild-type mice or mice overexpressing human wild-type LRRK2 exhibit long-term lipopolysaccharide-induced nigral neuronal loss. This neurodegeneration is accompanied by an exacerbated neuroinflammation in the brain,” write the investigators.

  “The increased immune response in the brain of mutant mice subsequently has an effect on neurons by inducing intraneuronal LRRK2 upregulation. However, the enhanced neuroinflammation is unlikely to be triggered by dysfunctional microglia or infiltrated T cells and/or monocytes, but by peripheral circulating inflammatory molecules. Analysis of cytokine kinetics and inflammatory pathways in the peripheral immune cells demonstrates that LRRK2 mutation alters type II interferon immune response, suggesting that this increased neuroinflammatory response may arise outside the central nervous system. Overall, this study suggests that peripheral immune signalling plays an unexpected—but important—role in the regulation of neurodegeneration in LRRK2-associated Parkinson’s disease, and provides new targets for interfering with the onset and progression of the disease.”

  "We know that brain cells called microglia cause the inflammation that ultimately destroys the area of the brain responsible for movement in Parkinson's," said Richard Smeyne, Ph.D., director of the Jefferson Comprehensive Parkinson's Disease and Movement Disorder Center at the Vickie and Jack Farber Institute for Neuroscience. "But it wasn't clear how a common inherited mutation was involved in that process, and whether the mutation altered microglia."

  Together with senior author Dr. Smeyne, first author Elena Kozina, Ph.D., looked at the mutant version of the LRRK2 gene. Mutations in the LRRK2 gene are the most common cause of inherited Parkinson's disease and are found in 40% of people of North African Arab descent and 18% of people of Ashkenazi Jewish descent with Parkinson's. However, there's been controversy around the exact function of the LRRK2 gene in the brain.

  "We know that gene mutation is not enough to cause the disease," said Dr. Kozina, a postdoc at Jefferson (Philadelphia University and Thomas Jefferson University). "We know that twins who both carry the mutation won't both necessarily develop Parkinson's. A second 'hit' or initiating event is needed."

  Based on his earlier work showing that the flu might increase risk of Parkinson's disease, Dr. Smeyne decided to investigate whether that second hit came from an infection. Suspecting that the LRRK2mutations might be acting outside of the brain, the researchers used the outer shell of bacteria (lippopolysaccharide, or LPS) that causes an immune reaction. LPS itself does not pass into the brain, nor do the immune cells it activates, which made it ideal for testing whether this second hit was acting directly in the brain.

  When the researchers gave the bacterial fragments to the mice carrying the two most common LRRK2gene mutations, the immune reaction became a cytokine storm, with inflammatory mediators rising to levels that three to five times higher than a normal reaction to LPS. These inflammatory mediators were produced by T and B immune cells expressing the LRRK2 mutation. 

  Despite the fact that LPS did not cross the blood–brain barrier, the researchers showed that the elevated cytokines were able to enter the brain, creating an environment that caused the microglia to activate pathologically and destroy the brain region involved in movement. 

  "Although more tests are needed to prove the link, as well as testing whether the same is true in humans, these findings give us a new way to think about how these mutations could cause Parkinson's," said Dr. Smeyne. "Although we can't treat people with immunosuppressants their whole lives to prevent the disease, if this mechanism is confirmed, it's possible that other interventions could be effective at reducing the chance of developing the disease."

  https://www.genengnews.com/gen-news-highlights/new-finding-on-parkinsons-gene-mutation-alters-view-of-what-causes-the-disease/81255613

Gocovri Significantly Improves Dyskinesia and ‘Off’ Time in Parkinson’s, New Analysis Confirms

MARCH 22, 2018 BY PATRICIA INACIO, PHD 

Parkinson’s disease patients treated with Gocovri (amantadine) experienced a 41 percent decrease in levodopa-induced dyskinesia compared to 14 percent of healthy people who took placebos.

That analysis of two Phase 3 trials are summarized in the study “Pooled Analyses of Phase III Studies of ADS-5102 (Amantadine) Extended-Release Capsules for Dyskinesia in Parkinson’s Disease,” published in the journal CNS Drugs.

“The results from this pooled analysis of two Phase 3 studies confirms the consistency of GOCOVRI’s benefit on dyskinesia and [off] time, as demonstrated in the individual studies across different Parkinson’s disease patient populations and all primary and secondary endpoint measures,” Lawrence W. Elmer, MD, PhD, of the University of Toledo, said in a press release. Elmer is the study’s lead author.

Researchers pooled the results of two trials — the EASE LID (NCT02136914) and the EASE LID 3 (NCT02274766 ) — that assessed the effectiveness of Adamas Pharmaceuticals’ Gocovri extended release capsules compared to placebo oral capsules in Parkinson’s disease patients with levodopa-induced dyskinesia, in which patients experience involuntary, jerky movements.

The trials’ design and eligibility criteria were the same in both Phase 3 trials, with the exception of treatment duration; in EASE LID patients underwent treatment for 25 weeks, and in EASE LID 3 the trial stopped at week 13.  Gocovri was given once every night at bedtime.

Researchers pooled the trial’s results to analyze its primary goal, which assessed changes in the Unified Dyskinesia Rating Scale (UDysRS) score from baseline to week 12.

Additional parameters included changes in the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale (MDS-UPDRS), patient-reported Parkinson’s disease home diary data, and Clinician’s Global Impression of Change (CGI-C) in Overall PD Symptoms.

Gocovri led to a 41.1% reduction in dyskinesia from baseline to week 12 in the UDysRS score compared to 13.9% for the placebo group — a significant difference of 27.2%.

Also, dyskinesia and “off” time (period when medication is not working efficiently) also was improved, with patients achieving almost a four-hour improvement in “on” time without so-called “troublesome” dyskinesia.

By week 12, 25% of the patients treated with Gocovri had a complete resolution of off time compared to 14% in the placebo group.

Also, 68% of patients in the Gocovri group had an increase of more than two hours a day of on time without troublesome dyskinesia versus 40% in the placebo group. Moreover, 52% of patients treated with Gocovri had a complete resolution of on time with troublesome dyskinesia compared to only 23% of the placebo group.

“Patients take Gocovri once-daily at bedtime, which provides them with high amantadine concentrations upon waking and throughout the day when dyskinesia and [off] occur, and then lower concentrations in the evening when amantadine can disrupt sleep patterns. What’s most important from this pooled analysis, is that over half of patients treated with GOCOVRI reported a complete resolution of their [on] time with troublesome dyskinesia at 12 weeks,” he added.

The researchers believe these data show further evidence to support Gocovri as an adjunct to levodopa to treat both dyskinesia and off time in Parkinson’s patients with dyskinesia.

“With its demonstrated, consistent clinical efficacy, Gocovri finally provides a solution for physicians and patients needing a proven durable treatment for dyskinesia in people with Parkinson’s disease,” said Rajiv Patni, MD, chief medical officer of Adamas Pharmaceuticals, Inc.

https://parkinsonsnewstoday.com/2018/03/22/adamas-announces-publication-of-data-supporting-the-benefits-of-gocovri-in-parkinsons-disease-patients-with-dyskinesia/

Calorie restriction trial in humans suggests benefits for age-related disease

March 22, 2018, Cell Press

This graphical abstract depicts the effects of a 2-year calorie restriction (CR) trial in healthy, non-obese humans, which found evidence that prolonged CR enhances resting energy efficiency, resulting in decreased oxidative damage to tissues and organs. Credit: Redman et al./Cell Metabolism

One of the first studies to explore the effects of calorie restriction on humans showed that cutting caloric intake by 15% for 2 years slowed aging and metabolism and protected against age-related disease. The study, which will appear March 22 in the journal Cell Metabolism, found that calorie restriction decreased systemic oxidative stress, which has been tied to age-related neurological conditions such as Alzheimer's and Parkinson's diseases, as well as cancer, diabetes, and others.

"Restricting calories can slow your basal metabolism, and if by-products of metabolism accelerate aging processes, calorie restriction sustained over several years may help to decrease risk for chronic disease and prolong life," says lead author Leanne M. Redman, associate professor of Clinical Sciences at Pennington Biomedical Research in Baton Rouge, LA.

CALERIE (Comprehensive Assessment of the Long-Term Effects of Reducing Intake of Energy) was the first randomized controlled trial to test the metabolic effects of calorie restriction in non-obese humans. The second phase of the study reports results from 53 healthy, non-obese men and women between ages 21 and 50 who cut calories by 15% over 2 years and underwent additional measurements for metabolism and oxidative stress. The calorie reductions were calculated individually through the ratio of isotopes absorbed by the participants' molecules and tissues over 2 weeks, a technique that accurately pinpoints a weight-maintenance calorie level.

Those in the calorie restriction group lost an average of almost 9 kg, although they did not follow a particular diet and weight loss was not the study's goal. No adverse effects, such as anemia, excessive bone loss, or menstrual disorders were noted; in fact, both trials led to improvements in mood and health-related quality of life. "We found that even people who are already healthy and lean may benefit from a calorie restriction regimen," Redman says.

In lab animals, calorie restriction lowers core body temperature and resting metabolic rate. Redman emphasized that CALERIE looked at the effects of calorie restriction on aging, not weight loss, where discussions of "fast" or "slow" metabolism most often arise. "We know from mammalian studies that the smaller the mammal, the faster their metabolism and the shorter their longevity," she says.

Many factors, such as antioxidant mechanisms and dietary and biological factors, influence metabolism, Redman says, but current theories hold that a slower metabolism is most beneficial for healthy aging and that organisms that burn energy most efficiently should experience the greatest longevity.

"The CALERIE trial rejuvenates support for two of the longest-standing theories of human aging: the slow metabolism 'rate of living' theory and the oxidative damage theory," she says. The latter ties overproduction of free radicals to oxidative damage to lipids, proteins, and DNA, leading to chronic diseases such as atherosclerosis, cancer, diabetes, and rheumatoid arthritis.

While the number of participants was relatively small and the duration short in the context of a human lifespan, biomarkers of aging were improved in study participants. Next steps include establishing robust biomarkers of human aging and examining the effects of calorie restriction in conjunction with antioxidant foods or substances like resveratrol, which mimic calorie restriction.

More information: Cell Metabolism, Redman et al. "Metabolic Slowing and Reduced Oxidative Damage with Sustained Caloric Restriction Support the Rate of Living and Oxidative Damage Theories of Aging." http://www.cell.com/cell-metabolism/fulltext/S1550-4131(18)30130-X,DOI: 10.1016/j.cmet.2018.02.019 

Journal reference: Cell Metabolism 

Provided by: Cell Press 

https://medicalxpress.com/news/2018-03-calorie-restriction-trial-humans-benefits.html

FoxFeed Blog: National Institutes of Health Receives $3 Billion Spending Boost

Posted by  Allyse Falce, March 22, 2018

Late last night, Congress released a spending deal (called an omnibus) to fund the government for the rest of Fiscal Year (FY) 2018, which runs until September 30, 2018. This bill must be passed by both chambers of Congress by the end of the day on Friday, March 23, when current funding levels expire.

The spending deal includes a $3 billion increase for the National Institutes of Health (NIH), which is the largest boost the agency has seen since FY 2003. The NIH is the largest public funder of Parkinson's research and its work is critical to furthering our understanding of the disease. However, the NIH is only able to support 12 percent of the grants it receives, leaving a significant percentage of scientific ideas unfunded. The $3 billion increase is key to helping the agency fuel research progress.

Thank you to each and every member of the Parkinson's community who spoke up for research funding and asked their lawmakers to raise the NIH budget. Members of Congress are listening, and they know that advancing better treatments and a cure is a priority to their constituents. Thank you for taking action.

Now, Congress will turn its attention to FY 2019 funding. Hundreds of Parkinson's advocates were in Washington, D.C. earlier this week to ask their lawmakers to continue increasing medical research funding in the next fiscal year, and individuals across the country sent their lawmakers thousands of emails on this topic. Stay tuned to our blog and your email inboxes for opportunities advocate for the Parkinson's community during the ongoing FY 2019 spending negotiations.

https://www.michaeljfox.org/foundation/news-detail.php?national-institutes-of-health-receives-billion-spending-boost

The Michael J. Fox Foundation Funds Three Research Teams to Seek Common Biological Pathways Underpinning Environment, Genetics and Aging in Parkinson's Onset and Progression

March 22, 2018
SOURCE The Michael J. Fox Foundation

$6-million, two-year program to holistically investigate known risk and causal factors toward discovery of common framework underlying onset and progression of Parkinson's disease

NEW YORK, March 22, 2018 /PRNewswire-USNewswire/ -- As part of its mission to accelerate the development of urgently needed treatment breakthroughs for Parkinson's disease (PD), The Michael J. Fox Foundation for Parkinson's Research (MJFF) announces a program investigating the pathogenesis of Parkinson's: PATH to PD. This ambitious multi-team, multi-million-dollar initiative aims to identify molecular/cellular events that may play a role in Parkinson's onset and progression, whether in the presence of environmental exposures, genetic factors and aging.

"The vast diversity of pathways implicated in Parkinson's pathology to date indicates that multiple physiological routes can lead to PD, and these routes may intersect or be temporally dependent," said Todd Sherer, PhD, MJFF CEO. "Through PATH to PD, our Foundation aims to encourage researchers to bring a holistic new approach to bear on refining today's understanding of what Parkinson's is - so that we can better strategize how to slow or stop the disease."

A Holistic Approach

Parkinson's arises from multiple, complicated gene-environment interactions on the poorly understood background of aging. The past two decades have brought substantial growth in understanding of the disease, in particular a strong appreciation of the role of genetics and the cellular pathways they influence. The emerging research picture of Parkinson's is that of a vast, interwoven network culminating in a disease with great variability in cause, rates of progression, symptomology and treatment responses. 

Each PATH to PD-funded research team will receive $2 million over two years to holistically investigate genetics, environment and aging, the most important known contributors to Parkinson's disease. Teams will look for a common framework that links mechanisms through which these risk and causal factors may lead to Parkinson's - independently and/or in concert with each other. Teams additionally will work to understand whether disease mechanisms at play in idiopathic forms of PD hew more closely to those seen in the presence of genetic abnormalities or environmental exposures. 

• Environmental and Genetic Mechanisms of Parkinson's will seek out links between environmental and genetic triggers of disease. This project will investigate the mechanisms through which neurotoxins cause neurodegeneration and how these pathways interact with known genetic factors such as LRRK2, a leading genetic cause of PD.
  
  
  "It is an honor to be selected by The Michael J. Fox Foundation to participate in this unique collaborative project. Our work focuses on the commonalities of Parkinson's disease causation, whether it's due to genetic mutations or environmental exposures. We hope that by defining these common mechanisms, we will know how best to intervene therapeutically to slow or stop disease progression," said Principal Investigator J. Timothy Greenamyre, MD, PhD, of the Pittsburgh Institute for Neurodegenerative Diseases and the University of Pittsburgh.
  
  
• Foundational Data Initiative: Mapping Genetic Effects in Parkinson's will grow nerve cells from induced pluripotent stem cells and use advanced "omics" techniques (e.g., genomics, proteomics, metabolomics) to map how various genetic changes lead to cellular and molecular changes associated with PD.
  
  
  "We are pleased to be part of a truly multidisciplinary group that brings together experts with a common goal to produce foundational data that will accelerate the field's ability to understand the disease processes and to find logical places for intervention," said Principal Investigator Andrew Singleton, PhD, of the National Institute on Aging, part of the National Institutes of Health.
  
  
• Aging and Parkinson's Disease will investigate how cellular aging and related DNA and mitochondrial damage contributes to neurodegeneration. Advanced gene-editing techniques will allow this team to investigate these processes in both rodent and human cells.
  
  
  "I'm honored and extremely grateful to MJFF for this award. It gives us the opportunity to do the kind of innovative, interdisciplinary science that can lead to conceptual breakthroughs and identification of the shortest possible path to a real strategy for stopping Parkinson's disease," said Principal Investigator D. James Surmeier, PhD, of Northwestern University.

A Complex Disease

While the Parkinson's drug development pipeline is brimming with greater activity than ever before, many unmet medical needs persist in the treatment and management of Parkinson's disease. The greatest of these remains the need for a so-called "disease-modifying" treatment, or one that could slow or stop the underlying progression of Parkinson's disease. This is something no currently available treatment has been proven to do. 

Researchers believe a disease-modifying treatment has the best chance for success if it targets key underlying pathogenic pathways implicated in the disease.  

Several dozen different gene mutations have been linked to inherited, familial PD, but the vast number of PD cases occur with no known gene mutation. The different genes linked to familial PD thus far lie in multiple, distinct pathways, including protein balance/recycling, cellular energy metabolism, stress response, neurotransmission and inflammation/immune function, among others. 

Environmental factors associated with heightened risk of PD include previous head injury, heavy metal exposure, pesticide exposure and previous brain infection. 

Above all, aging is the single greatest risk factor for PD, which implicates either physiological changes that occur naturally with advanced age or a lifetime accumulation of otherwise minor environmental exposures that either themselves accumulate and eventually lead to development of PD or contribute to "turn on" PD risk genes - or a combination of both. 

"With Parkinson's prevalence expected to double by 2040 to nearly 13 million people worldwide, our Foundation believes it is our obligation to continue building on current research momentum to eradicate this disease once and for all," concludes CEO Sherer. "We are grateful to our supporters, many living with Parkinson's disease, whose generosity enables us to drive innovation toward breakthroughs through programs like PATH to PD."

About The Michael J. Fox Foundation for Parkinson's Research

As the world's largest nonprofit funder of Parkinson's research, The Michael J. Fox Foundation is dedicated to accelerating a cure for Parkinson's disease and improved therapies for those living with the condition today. The Foundation pursues its goals through an aggressively funded, highly targeted research program coupled with active global engagement of scientists, Parkinson's patients, business leaders, clinical trial participants, donors and volunteers. In addition to funding more than $800 million in research to date, the Foundation has fundamentally altered the trajectory of progress toward a cure. Operating at the hub of worldwide Parkinson's research, the Foundation forges groundbreaking collaborations with industry leaders, academic scientists and government research funders; increases the flow of participants into Parkinson's disease clinical trials with its online tool, Fox Trial Finder; promotes Parkinson's awareness through high-profile advocacy, events and outreach; and coordinates the grassroots involvement of thousands of Team Fox members around the world. 

For current funding opportunities, visit www.michaeljfox.org/funding. 

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