Monthly Archives: październik 2014

Researchers studying frontotemporal degeneration (FTD) disease, a leading cause of early onset dementia, will receive more than $30 million over the next five years in grants from the National Institutes of Health (NIH). The funding will be used to further scientific collaboration and investigate new treatments in the quest to find a cure for FTD.

Also, in Vancouver, Canada, on October 23rd, an FTD conference demonstrated the research progress made in this awakening field, with particular emphasis on the newly forged international collaborative relationships to comprehensively examine patients and their families in longitudinal cohort studies.

A total of fifteen international consortia have been proposed for funding under two JPND Transnational calls between a total of 18 countries.

These new projects are aiming to analyse neurodegenerative diseases across traditional clinical boundaries, and also to begin “pilot” studies for the design of preventive strategies.

The projects are supported under two JPND transnational calls for proposals entitled:

The calls were launched in December 2013 with a pre-proposal deadline of March 2014. Sixteen countries participated in each call.

The project proposals have been proposed for funding by the respective Peer Review Panels based on scientific evaluation and by the respective Call Steering Committees based on budget availability.

For further information on the projects proposed for funding, click on the links below.

In the first post on this new online service, Dr Ed Wild and Dr Jeff Carroll talk about the five new clinical trials enrolling now or starting soon for Huntington’s disease. Plus, a detailed discussion of the eagerly-awaited clinical trial of the first 'huntingtin lowering’ drug to be tested in Huntington’s diease. Called HTT-Rx, the drug is an antisense oligonucleotide developed by Isis Pharmaceuticals Inc.

In the UK, to support clinical and care staff, managers and estates colleagues, the King’s Fund has produced a range of resources to enable hospitals, care homes, primary care premises and specialist housing providers to become more dementia friendly.

The work that informed the initial development of the resources, the EHE dementia care programme, was funded by the Department of Health to support the implementation of the National Dementia Strategy and the Prime Minister’s ‘Challenge on Dementia’.

The EHE programme is designed to improve the environment of care for people with dementia. It involved 23 teams from acute, community and mental health NHS trusts who worked on a range of projects across the dementia care pathway and sought to make hospital environments less alienating for people with cognitive problems. Projects have demonstrated that relatively inexpensive interventions, such as changes to lighting, floor coverings and improved way-finding, can have a significant impact. Evaluation has shown that environmental improvements can have a positive effect on reducing falls, violent and aggressive behaviours, and improving staff recruitment and retention. The EHE schemes are already showing that it is possible to improve the quality and outcomes of care for people with dementia as well as improve staff morale and reduce overall costs by making inexpensive changes to the environment of care.

The King’s Fund has also published on Sept. 4th 2014, the final report of the Commission on the Future of the Health and Social Care in England (the Barker report).  A New Settlement for Health and Social Care, relations between health and social services”, makes a plea for “better integration” and warns of “hard choices” ahead.

The 2014 Nobel Prize in Physiology or Medicine has honored three neuroscientists.

John O’Keefe, along with May-Britt Moser and Edvard Moser, discovered cells that form a positioning system in the brain — our hard-wired GPS. Those cells mark our position, navigate where we’re going and help us remember it all, so that we can repeat our trips, the Nobel Assembly said in a statement.

Their research could also prove useful in Alzheimer’s research, because of the parts of the brain those cells lie in — the hippocampus and the entorhinal cortex.

Humans and other mammals have two hippocampi, which lie in the inner core of the bottom of the brain and are responsible for memory and orientation. The entorhinal cortices share these functions and connect the hippocampi with the huge neocortex, the bulk of our gray matter.

In Alzheimer’s patients, those two brain components break down early on, causing sufferers to get lost more easily. Understanding how the brain’s GPS works may help scientists in the future understand how this disorientation occurs.

The research is also important, because it pinpoints „a cellular basis for higher cognitive function,” the Nobel Assembly said.

The scientists conducted their research on rats, but other research on humans indicates that we have these same cells.

A Small Number of Patients With Fetal-Cell Transplants Are Thriving Two Decades Later.

Several patients with Parkinson’s disease who received brain-tissue transplants from fetuses in the early 1990s have needed little or no medicine to treat the disease ever since—an outcome virtually unheard of in the course of the disease, researchers have found.

The results are particularly striking because the treatment is controversial and has been questioned by some researchers in the field.

Bolstered by these promising cases, 14 European hospitals, research institutions and companies have launched a new, controversial trial on fetal-cell transplants, known as Transeuro. Funded with a $15 million grant by the European Union, surgeons in Cambridge, England, are expected to perform their first transplant on a trial participant by year’s end. It would be the first since the 1990s.

Scientists studying two genes that are mutated in an early-onset form of Parkinson’s disease have deciphered how normal versions of these genes collaborate to help rid cells of damaged mitochondria.

Mitochondria are the cell’s primary energy source, and maintaining their health is critical for cellular function. Mitochondrial dysfunction may underlie multiple neurodegenerative diseases, including Parkinson’s.

In their analysis published in Molecular Cell, Harvard Medical School researchers used powerful quantitative mass spectrometry and live-cell imaging approaches to elucidate a multistep mechanism by which the two proteins mutated in Parkinson’s disease—PINK1 and PARKIN—mark mitochondria as damaged by attaching chains of a small protein called ubiquitin. This work paves the way for a deeper understanding of what molecular steps are defective when these proteins are mutated in patients with Parkinson’s disease.

Just three months after a paper outed a gene for a mitochondrial protein as a potential cause of amyotrophic lateral sclerosis-frontotemporal dementia, four new publications have made the case clear. CHCHD10 is an ALS/FTD spectrum gene.

A handful of different mutations in the gene (whose acronym stands for the tongue twister coiled-coil-helix-coiled-coil-helix domain containing 10) cause a range of symptoms comprising ALS-FTD, ALS, and also mitochondrial myopathy, according to the studies.

The Walk On Project (WOP) has the aim of publicizing, raising awareness, and assisting in the research of “rare” neurodegenerative diseases.

The 2014 WOP Call for research proposals has been extended and is now open until 20th October, 2014.

The objective of the call is the development of regeneration therapies based upon pre-existing technologies making it possible for short term application to patients. Projects should focus on research in short-term developable therapies on neurodegenerative diseases with special emphasis on de-myelinisation damage and neuro-apoptosis.