Yearly Archives: 2015

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 News.net

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.

Since late 2014, a total of 25 JPND-supported transnational projects and working groups have begun their work to tackle the challenge of neurodegenerative diseases in a number of JPND priority areas.

JPND has now published user-friendly fact sheets of the individual projects and working groups which are supported under the following previously-launched JPND calls for research proposals.

2014 Call for working groups on longitudinal cohort studies

2013 Call for pilot preventive strategies

2013 Call for cross-disease analysis of molecular pathways

The fact sheets are available on the particular call results page via the links above or through the “Supported Projects” section of the JPND website.

On January 26th, 2015, Switzerland joined the recently-launched ‘JPco-fuND’ call for proposals.

Researchers from Switzerland are now able to participate as external collaborators in proposals submitted to this call under all three call topics.

Specific conditions will apply and can be found on the “Specific regulations” page of the call.

Should a proposal involving a collaboration with Switzerland be recommended for funding, this collaboration will be eligible for funding by the Swiss National Science Foundation.

Belgian scientists have completed a study, reprogramming skin cells from three dementia patients into induced pluripotent stem cells (iPSCs) – immature cells that mimic stem cells taken from early-stage embryos. Their findings, which revealed a signalling pathway linked to frontotemporal dementia (FTD), are published in the January 13th 2015 edition of the journal, Stem Cell Reports.

Prof. Philip Van Damme, from the Leuven Research Institute for Neuroscience and Disease in Belgium, said: “Our findings suggest that signalling events required for neurodevelopment may also play major roles in neurodegeneration.

Treatment with a drug that suppressed the pathway, known as “Wnt”, restored the ability of neurons affected by the disease to develop normally. “Targeting such pathways…may result in the creation of novel therapeutic approaches for frontotemporal dementia”, Prof. Van Damme said.

The researchers found that iPSCs derived from the patients’ cells were unable to generate cortical neurons, the cell type most affected by FTD. Cortical neurons are the cells responsible for most of the brain’s complex higher activity enabling thought, perception and voluntary movement.

Co-author Dr Catherine Verfaillie, from the University of Leuven in Belgium commented that IPSC models could now be used to better understand dementia, and in particular FTD, which accounts for about half of dementia cases before the age of 60.

Source: Alzheimer Europe