Tag Archives: MND

The EU Joint Programme – Neurodegenerative Disease Research (JPND) has announced a rapid-action call inviting leading scientists in the field to bring forward novel approaches that will enhance the use of brain imaging for neurodegenerative disease research.

Imaging techniques such as MR, PET and EEG mapping have brought about a dramatic improvement in the understanding of neurodegenerative diseases such as Alzheimer’s disease. In recent years, access to cutting-edge imaging technologies and platforms has expanded, and advances have been made in the harmonisation of acquisition procedures across scanners and vendors. However, fully capitalising on the use of brain imaging technologies for neurodegeneration research will require the development of new methodologies and the ability to achieve image acquisition and analysis at scale and at the global level.

The aim of the call is to establish a limited number of transnational working groups to address the key challenges facing the use of new and innovative brain imaging techniques in neurodegenerative disease research. The working groups will be community-led and will establish ‘best practice’ guidelines and/or methodological frameworks to overcome these barriers. Each working group can bid up to €50,000 for the support of its activities, which are expected to run for a maximum of 9 months.

According to Professor Philippe Amouyel, Chair of the JPND Management Board:

“JPND recognises that state-of-the-art brain imaging techniques are a vital resource for neurodegenerative disease research. However, achieving scalability for these technologies poses new challenges. For this reason, we’ve launched a rapid-action call inviting international research teams to address the most urgent issues in harmonisation and alignment in neuroimaging. The establishment of effective new guidelines and methodological frameworks will represent a critical step toward the full exploitation of brain imaging in neurodegenerative disease research.”

The following neurodegenerative diseases are included in the call:

  • Alzheimer’s disease and other dementias
  • Parkinson’s disease and PD‐related disorders
  • Prion diseases
  • Motor neuron diseases
  • Huntington’s disease
  • Spinocerebellar ataxia (SCA)
  • Spinal muscular atrophy (SMA)

Proposals must be submitted by 23:59H C.E.T. on March 10, 2016.

For more information about the call, please click here.

 

Using data from old clinical trials, two groups of researchers have found a better way to predict how amyotrophic lateral sclerosis (ALS) progresses in different patients. The winning algorithms—designed by non-ALS experts—outperformed the judgments of a group of ALS clinicians given the same data. The advances could make it easier to test whether new drugs can slow the fatal neurodegenerative disease.

The new work was inspired by the so-called ALS Prediction Prize, a joint effort by the ALS-focused nonprofit Prize4Life and Dialogue for Reverse Engineering Assessments and Methods (DREAM), a computational biology project whose sponsors include IBM and Columbia University. Announced in 2012, the $50,000 award was designed to bring in experts from outside the ALS field to tackle the notoriously unpredictable illness.

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.

Twins who came to an ALS Clinic in Toronto were identical down to the repeats in their C9ORF72 genes, except one had amyotrophic lateral sclerosis and the other did not. The mismatch suggests environmental influences modified the twins’ risk for ALS, researchers concluded in the September 10 Neurology online.

More studies of identical twins with C9ORF72 repeats should help scientists identify such factors, said Ekaterina Rogaeva of the University of Toronto, senior author on the report.

Co-senior author Lorne Zinman of the Sunnybrook Health Sciences Centre in Toronto examined the women, who are now 62. One developed motor neuron symptoms at age 57, although she performed normally on cognitive tests. Her sister shows no signs of ALS.

However, the unaffected twin performed poorly on some cognitive tests and though her scores were not low enough to conclude she has frontotemporal dementia (FTD), they suggest she might be headed in that direction, said Rogaeva.