A more intensive exercise program specifically designed for people in hospital with dementia has been shown to add benefits over normal rehabilitation.
The study was published in theFebruary 2014 issue of the Journal of Alzheimer’s Disease (requires subscription to view full article).
A pre-press version of An Intensive Exercise Program Improves Motor Performances in Patients with Dementia: Translational Model of Geriatric Rehabilitation at the links below:
The underlying genetics of neurodegenerative disorders tend not to be well understood. This study links HSP to other neurodegenerative disorders and can potentially facilitate further gene discovery and mechanistic understanding of neurodegenerative diseases.
Hereditary spastic paraplegias (HSPs) are neurodegenerative motor neuron diseases characterized by progressive age-dependent loss of corticospinal motor tract function.
In this study, researchers investigated the underlying genetics of hereditary spastic paraplegia (HSP), a human neurodegenerative disease, by sequencing the exomes of individuals with recessive neurological disorders. Loss-of-function gene mutations in both novel genes and genes previously implicated for this condition were identified, and several were functionally validated.
Source: Science Magazine (requires subscription to view full article)
The word “chaperone” refers to an adult who keeps teenagers from acting up at a dance or overnight trip. It also describes a type of protein that can guard the brain against its own troublemakers: misfolded proteins that are involved in several neurodegenerative diseases.
Researchers at Emory University School of Medicine have demonstrated that as animals age, their brains are more vulnerable to misfolded proteins, partly because of a decline in chaperone activity.
The researchers were studying a model of spinocerebellar ataxia, but the findings have implications for understanding other diseases, such as Alzheimer’s, Parkinson’s and Huntington’s.
They also identified targets for potential therapies: bolstering levels of either a particular chaperone or a growth factor in brain cells can protect against the toxic effects of misfolded proteins.
The results were published in the journalNeuron.
Source: Medical Express
A number of studies have shown that exercise can remodel the brain by prompting the creation of new brain cells and inducing other changes. Now it appears that inactivity, too, can remodel the brain, according to a new report.
The study, which was conducted in rats but likely has implications for people too, the researchers say, found that being sedentary changes the shape of certain neurons in ways that significantly affect not just the brain but the heart as well. The findings may help to explain, in part, why a sedentary lifestyle is so bad for us.
Source: New York Times Blogs
The phase 3 trial results of Eli Lilly and Co.’s solanezumab and Janssen/Pfizer’s bapineuzumab appeared in the January 23rd edition of the New England Journal of Medicine.
In an accompanying editorial in NEJM, JPND Scientific Advisory Board members Eric Karran of Alzheimers Research U.K., and John Hardy of University College London (neither of whom were involved in the trials), gave their insights into the results.
Both monoclonal antibodies failed to slow cognitive or functional decline in patients with mild to moderate Alzheimers disease. However, each drug hinted at smaller benefits and bolstered the idea that amyloid-related treatments, if they are to work, must be applied early in the disease process, perhaps before cognitive symptoms emerge.
Source: AlzForum
Researchers at Duke University have shown that continuing spinal cord stimulation appears to produce improvements in symptoms of Parkinson’s disease, and may protect critical neurons from injury or deterioration.
The study, performed in rats, is published online Jan. 23, 2014, in the Journal "Scientific Reports". It builds on earlier findings from the Duke team that stimulating the spinal cord with electrical signals temporarily eased symptoms of the neurological disorder in rodents.
Source: Medical Express
New research has uncovered a quality-control mechanism in brain cells that may help keep deadly neurological diseases in check for months or years.
The findings, published in The Journal of Clinical Investigation, present a breakthrough in understanding the secret life of prion molecules in the brain and may offer a new way to treat prion diseases, said David Westaway, director of the Center for Prions and Protein Folding Diseases at the University of Alberta.
Prion diseases lead to incurable neurodegenerative disorders such as Creutzfeldt-Jakob disease in humans, mad cow disease (Bovine Spongiform Encephalopathy) and chronic wasting disease in deer and elk. The diseases are caused by the conversion of normal cellular prion proteins into the diseased form.
For years, scientists have been perplexed by two unexplained characteristics of prion infections: vastly differing asymptomatic periods lasting up to five decades, and when symptoms do arise, greatly varying accumulation of the diseased proteins. In striking contrast, test tube prions replicate rapidly, and in a matter of days reach levels found in brains in the final stage of the disease.
Our study investigated the molecular mechanism of this intriguing puzzle, said Jiri Safar, co-director of the National Prion Disease Pathology Surveillance Center. In probing these mysteries, Westaway, Safar, their teams and other collaborating researchers in the U.S., Italy and the Netherlands studied a molecule called the shadow of the prion protein.
Dramatic changes in this shadow protein led us to expand our view to include the normal prion protein itself, said Westaway. This is a crucial molecule in brain cells because it is pirated as the raw material to make diseased prion proteins.
From: Case Western Reserve University
The Innovative Medicines Initiative (IMI) launched its 11th call for proposals on December 11th, 2013. The call features eight topics including the “European platform for proof of concept for prevention in Alzheimers Disease” (EPOC-AD).
EPOC-AD calls for greater cooperation and collaboration between academia, government and industry to enhance the drug development process.
The project would create a precompetitive space to enable collaboration for optimising patient selection, clinical trials methodologies and candidate therapies, as well as conducting adaptive clinical trials that will produce the greatest likelihood of success.
A declaration and a communique present the agreements consolidated at the G8 Dementia Summit in London on December 11th, 2013.
G8 countries have agreed:
An Alzheimer Disease International (ADI) policy brief entitled The Global Impact of Dementia 2013-2050 has revealed a staggering 17% increase in the number of people living with dementia, compared to the original ADI estimates in the 2009 World Alzheimer Report.
The first G8 Dementia Summit took place in London, UK, on 11 December. The summit will aim to identify and agree a new international approach to dementia research and policy.
This Alzheimer Disease International brief for the summit reveals that the number of people living with dementia worldwide in 2013 is now estimated at 44 million, reaching 76 million in 2030 and 135 million by 2050.
The report also predicts a shift in the distribution of the global burden of dementia. Where previously high income countries have witnessed the strongest visible trends, it will now be low and middle income countries who will feel the heaviest burden. By 2050, 71% of people with dementia will live in low and middle income countries.