Monthly Archives: luty 2015

On February 26th, 2015, Australia joined the ‘JPco-fuND’ call for proposals.

Due to this late arrival, researchers from Australia can participate as external collaborators in proposals submitted to this call under specific conditions.

The specific conditions for researchers in Australia can be found on the “Specific regulations” page of the call.

Should a proposal involving a collaborator from Australia be recommended for funding, these collaborators are eligible for funding from the NHMRC National Institute of Dementia Research (NNIDR).

*Please Note: Under this call the NNIDR will only fund research that focusses primarily on Alzheimer’s disease and other dementias.

The Joint Programming Initiative “A Healthy Diet for A Healthy Life” is launching a new joint transnational call for research proposals on “Nutrition and Cognitive Function”.

The call aims to support small transnational research consortia with innovative and interdisciplinary approaches tackling the interrelationships between nutrition and cognition.

The call is scheduled to be launched on March-30, 2015 with the deadline for proposal submission scheduled for June 8th, 2015.

The pre-call announcement is available here and through the link below:


The March 2015 editorial of The Lancet Neurology is entitled „Teaming up to fight neurodegenerative diseases„.

The editorial focuses on the recently-launched JPcofuND initiative.

To view the editorial, click here or on the link below.

The latest media articles on JPND (including previous Lancet Neurology editorials) are available here.



Image courtesy of The Lancet Neurology.

A study published in the journal Human Mutation revealed new genetic mutations in a domain of a dynein gene. The study, entitled “Novel mutations in the DYNC1H1 tail domain refine the genetic and clinical spectrum of dyneinopathies,” unlocks new insights into motor neuron diseases such as Spinal Muscular Atrophy.

Dynein is a microtubule motor protein that uses the energy contained in ATP (adenosine triphosphate) molecules to move. Dyneins can be either axonemal, facilitating the movement of cilia and flagella, or cytoplasmic, transporting several intracellular cargos along microtubule tracks. The movement of cytoplasmic dyneins is usually directed towards the center of the cell.

Several studies show evidence that genetic mutations in dyneins underlie some neurodegenerative disorders such as Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, and motor neuron diseases.

Source:  SMA News Today

The Accelerating Medicines Partnership (AMP) is a new venture between the US National Institutes for Health (NIH), 10 bio-pharmaceutical companies and several non-profit organizations to transform the current model for developing new diagnostics and treatments by jointly identifying and validating promising biological targets of disease. The ultimate goal is to increase the number of new diagnostics and therapies for patients and reduce the time and cost of developing them.

AMP will begin with three to five year pilot projects in three disease areas: Alzheimer’s Disease, type 2 diabetes and autoimmune disorders of rheumatoid arthritis and systemic lupus erythematosus (lupus).

Focus on Alzheimer’s Disease:

For the project on biomarkers, the tau imaging and EEG data will be released in year two, as baseline data become available. Final data from the randomized, blinded trials will be added after the end of the five year studies, and will include both the imaging data and data from blood and spinal fluid biomarker studies. For the network analysis project, each individual project will generate several network models of late onset AD (LOAD) and will identify key drivers of disease pathogenesis by the end of year three. Years four and five will be largely dedicated to validating the novel targets and refining the network models of LOAD, including screening novel compounds or drugs already in use for other conditions that possess the ability to modulate the likely targets.

The budget for Alzheimer’s Disease over 5 years is $129.5 Million (Total Project Funding)

Source:  NIH (USA)


Creatine monohydrate doesn’t appear to slow the progression of Parkinson’s disease, according to research published in the February 10 issue of the Journal of the American Medical Association (JAMA).

The new study included 1,741 people in the United States and Canada who had been diagnosed with Parkinson’s disease within the previous five years. All were receiving treatment for Parkinson’s disease. As part of the study, they were randomly assigned to take creatine monohydrate or a placebo in addition to their usual treatment.

The patients were enrolled from March 2007 to May 2010 and followed up until September 2013. The study was halted early because those taking creatine showed no differences in disease progression compared to those taking the placebo.

„These findings do not support the use of creatine monohydrate in patients with Parkinson’s disease,” study author Karl Kieburtz, MD, MPH, of the University of Rochester in New York, and colleagues write.

Source:  eMPR

SuperAgers have distinctly different looking brains than those of normal older people, and the same memory capacity as a younger person. Understanding their unique brains could lead to new treatments for dementia, researchers say.

Published Jan. 28 in the Journal of Neuroscience, a new study is the first to quantify brain differences of SuperAgers and normal older people.

Cognitive SuperAgers’ unusual brain signature has three common components when compared with normal persons of similar ages: a thicker region of the cortex; significantly fewer tangles (a primary marker of Alzheimer’s disease) and a whopping supply of a specific neuron –von Economo — linked to higher social intelligence.

'The brains of the SuperAgers are either wired differently or have structural differences when compared to normal individuals of the same age,’ said Changiz Geula, study senior author and a research professor at the Cognitive Neurology and Alzheimer’s Disease Center. 'It may be one factor, such as expression of a specific gene, or a combination of factors that offers protection.’

Source: Northwestern university

Three leading research funders from the UK and North America have joined forces to launch a new global initiative called MEND or, MEchanisms of cellular death in NeuroDegeneration, with a fund of $1.25 million USD for targeted research into brain diseases that cause dementia, such as Alzheimer’s.

Alzheimer’s Research UK, the Alzheimer’s Association based in the U.S. and the Weston Brain Institute in Canada, whose participation in MEND is funded by Selfridges, announce the collaboration in response to the G7 health leaders’ commitment to collectively and significantly increase funding for dementia research, as announced at their December 2013 summit. G7 health leaders met in Bethesda, Maryland (U.S.A), last week to review progress on their goal to identify a cure or disease-modifying treatment by 2025.

MEND is open to applications from scientists around the globe, and researchers will be encouraged to collaborate on projects, sharing knowledge and resources in order to speed up progress. It’s hoped the scheme will also help answer fundamental questions about the similarities and differences between different diseases, such as whether the underlying mechanisms that cause cell death differ from one disease to another, and why each disease affects different types.

Source:  Medical

According to a recent study from a team of researchers at Tel Aviv University, a mutation in a specific neuroprotective protein called ADNP has different expressions between males and females. This research adds new insights to what is currently known about the etiology of autism and Alzheimer’s disease. The results are published in the journal Translational Psychiatry.

Recent evidence suggests that ADNP has a neuroprotective effect in patients with autism spectrum disorder (ASD), and has also been found to be decreased in the serum of patients with Alzheimer’s disease (AD)

In the study entitled “Activity-dependent neuroprotective protein (ADNP) exhibits striking sexual dichotomy impacting on autistic and Alzheimer’s pathologies”, the research team found that the ADNP exhibits different activities in males and females, which implies that there are gender differences in the risk of developing certain diseases. While it has already been established that autism affects more males, and that Alzheimer’s disease tends to affect more females, these specific gender disparities remain minimally understood.

In a recent news release, Tel Aviv University’s Prof. Illana Gozes said, “If we understand how ADNP, an activity-related neuroprotective protein which is a major regulatory gene, acts differently in males and females, we can try to optimize drugs for potential future therapeutics to treat both autism and Alzheimer’s disease.”

Prof. Gozes and colleagues investigated gender differences in behavioral responses in mice with ADNP-altered and normal mice, to different cognitive challenges and social situations. The researchers observed learning and memory differences between female and male mice, especially in the hippocampus. The results indicate differences in ADNP expressions, which can result in ADNP-controlled autism and in genes that elevate one’s risk for Alzheimer’s disease.

“ADNP may be new to the world of autism, but I have been studying it for 15 years,” said Prof. Gozes. “Its gender-dependent expression changes male and female chemical tendencies toward different neurological disorders. Male and female mice may look the same and their brains may look the same, but they are not. When the expression of ADNP is different, it may cause different behaviors and different cognitive abilities. This study emphasizes the need to analyze men and women separately in clinical trials to find cures for diseases because they may respond differently.”

Source:  Alzheimer’s News Today

With several therapeutic approaches in development for Huntington’s disease, there is a need for easily accessible biomarkers to monitor disease progression and therapy response.

Researchers at Leiden University Medical Center in The Netherlands have discovered a panel of five genes whose expression in whole blood correlates with progression of Huntington’s disease.

In a study published in The European Journal of Human Genetics, the group reported that transcriptome analysis of 91 Huntington’s mutation carriers, about one third of whom were presymptomatic, and 33 controls yielded 167 differentially expressed genes. Twelve of the top 20 genes were validated using a different technique, and five of these proved significant in a smaller, independent cohort as well.

The authors suggest a first empiric formula predicting total motor score from the expression levels of our biomarker panel. Their data supports the view that peripheral blood is a useful source to identify biomarkers for Huntington’s disease and monitor disease progression in future clinical trials.