In 2015, JPND has launched a joint transnational co-funded call in partnership with the European Commission under the ERA-NET Co-fund scheme in three JPND priority areas:
Longitudinal Cohort Approaches, Advanced Experimental Models, Risk and Protective Factors.
Twenty-one project proposals are recommended for funding by the Peer Review Panel based on scientific excellence and by the Call Steering Committee based on budget availability.
More information here
JPND call 2014: “ Working Groups to Inform Cohort Studies in Neurodegenerative Disease Research“
Increasing the impact of longitudinal population studies for neurodegenerative disease research
The use of population studies offers a significant opportunity for research into factors affecting risk and progression of neurodegenerative disease, an opportunity that is greater than ever given the emergence of new molecular and digital technologies. However, to fully realise this potential there is a need to harmonise approaches and encourage collaboration and data sharing. In response to this, JPND commissioned ten groups of experts through a peer reviewed call for proposals to address methodological challenges preventing current population- and disease-based longitudinal cohorts being fully used for ND research. A brief description of the valuable reports and recommendations provided by each group is provided below.
Philippe Amouyel, the Chair of JPND comments:
JPND recognises that longitudinal cohort studies are a rich but under-used resource. This is why we designed a rapid-action call to ask leading international experts to put their heads together to help exploit this opportunity and make population studies more accessible to a wider range of researchers. The guidelines that have been provided through this extensive body of work provide an important resource for the scientific community, which will help researchers increase collaborative activity and make productive use of longitudinal cohort studies.
Reports available here
The topics for the 5th IMI-2 Call are confirmed and the call is open
The topics for the 5th Call under the Innovative Medicines Initiative 2 are now confirmed, with a heavy emphasis on Alzheimer’s Disease (AD). The following four AD-related topics are included in the call:
– Inflammation and Alzheimer’s disease (AD): modulating microglia function – focussing on TREM2 and CD33
– Understanding the role of amyloid biomarkers in the current and future diagnosis and management of patients across the spectrum of cognitive impairment (from pre-dementia to dementia)
– Evolving models of patient engagement and access for earlier identification of Alzheimer’s disease: phased expansion study
– Apolipoprotein E (ApoE) biology to validated Alzheimer’s disease targets
The call is now open for stage 1 proposals with a deadline of October 13th, 2015. More information is available at the links below:
Links:
Call overview: http://www.imi.europa.eu/content/imi-2-call-5-0
Stage 1 proposals: http://www.imi.europa.eu/content/stage-1-16
The COEN initiative has released its third call for proposals aiming to further catalyse collaborative research to drive a step change in neurodegeneration research.
The Network of Centres of Excellence in Neurodegeneration (COEN) initiative aims to build collaborative research activity in neurodegeneration research across borders, focusing on critical mass and excellence. COEN is aligned with JPND, although it operates as an independent entity.
The third COEN call for research proposals was recently launched by six of the eight COEN members and will provide funds for ‘Pathfinder’ grants for innovative research to underpin new approaches to therapeutic intervention.
As in previous COEN calls, applications will connect centres with a critical mass of resources and expertise to drive a step change in neurodegeneration research. The six agencies are contributing £4.0m to fund awards made under the call involving their national Centres of Excellence.
The remit of the call is broad in scope: projects may include studies to illuminate our understanding of neurodegenerative mechanisms, or create technological advances to support novel diagnostic or therapeutic approaches.
The call will be administered as for the previous COEN pathfinder call, with partners funding research in their own country. The list of awards made under the first two COEN calls is located here.
More information can be found at the COEN website at the link below. Closing date for submissions is 4pm on the 5th of October 2015 (BST; GMT+1)
The Alzheimer’s Association International Conference® (AAIC) is the world’s largest forum for the dementia research community. the 2015 conference takes place in Washington DC between July 18-23rd.
International investigators, clinicians and care providers gather annually to share the latest study results, theories and discoveries to bring the world closer to breakthroughs in dementia science.
As part of the Alzheimer’s Association’s research program, AAIC serves as a catalyst for generating new knowledge about dementia and fostering a vital, collegial research community.
The programme for this year’s meeting is available at the link below.
Research has uncovered further evidence of a system in the brain that persistently maintains memories for long periods of time. And paradoxically, it works in the same way as mechanisms that cause mad cow disease and other degenerative brain diseases.
In four papers published in Neuron and Cell Reports, researchers show how prion-like proteins – similar to the prions behind mad cow disease in cattle and Creutzfeld-Jakob disease in humans – are critical for maintaining long-term memories in mice, and probably in other mammals. The lead authors of the four papers are Luana Fioriti, Joseph Stephan, Luca Colnaghi and Bettina Drisaldi.
When long-term memories are created in the brain, new connections are made between neurons to store the memory. But those physical connections must be maintained for a memory to persist, or else they will disintegrate and the memory will disappear within days.Many researchers have searched for molecules that maintain long-term memory, but their identity has remained elusive.These memory molecules are a normal version of prion proteins, according to new research.
In one of many experiments described in the paper by Luana Fioriti, the researchers challenged mice to repeatedly navigate a maze, allowing the animals to create a long-term memory. But when the researchers knocked out the animal’s CPEB3 gene two weeks after the memory was made, the memory disappeared.
The researchers then discovered how CPEB3 works inside the neurons to maintain long-term memories. “Like disease-causing prions, functional prions come in two varieties, a soluble form and a form that creates aggregates,” said. Kandel. “When we learn something and form long-term memories, new synaptic connections are made, the soluble prions in those synapses are converted into aggregated prions. The aggregated prions turn on protein synthesis necessary to maintain the memory.”
As long as these aggregates are present, Kandel says, long-term memories persist. Prion aggregates renew themselves by continually recruiting newly made soluble prions into the aggregates. “This ongoing maintenance is crucial,” said Dr. Kandel. “It’s how you remember, for example, your first love for the rest of your life.”
A similar protein exists in humans, suggesting that the same mechanism is at work in the human brain, but more research is needed. “It’s possible that it has the same role in memory, but until this has been examined, we won’t know,” said Dr. Kandel. “There are probably other regulatory components involved,” he added. “Long-term memory is a complicated process, so I doubt this is the only important factor.
Source: Medical News Net
Beyond the four-letter alphabet of the genome, a far richer code dictates when and where genes are transcribed. The epigenome—defined by an ever-expanding list of modifications to DNA and the proteins that interact with it—determines which genes are dialed up or down and gives each cell type its unique personality. Thickening an already dense plot, three recent papers suggest that the brain may have its own epigenetic lingo.
One, published in Neuron on June 17, described the epigenome of three different types of neuron from the mouse brain—one excitatory, and two inhibitory. Among a slew of other findings, the study reported that neurons harbor a striking degree of cytosine methylation beyond the well-known cytosine-guanine (CpG) sites. This novel modification more closely correlated with gene expression and with neuronal phenotype than did the more common CpG methylation.
To generate a more detailed epigenetic map of neurons in the mouse brain, the researchers employed a technique called INTACT (isolation of nuclei tagged in specific cell types) to study nuclei from three types of neuron (see image above). The technique, which uses antibodies to capture nuclei expressing a protein tag, had been established in a plant model, and later used in flies, worms, and frogs, but never in mammals. INTACT isolates nuclei from homogenized tissue that is first frozen intact. This eliminates the need to first separate or sort the different types of cells, which can damage and/or activate neurons and confound results. INTACT allows researchers to obtain enough genetic material from specific cell types to run methylation and other epigenetic analyses.
Source: AlzResearch Forum
Scientists still do not know why some people develop Parkinson’s disease. Now researchers from Aarhus University and Aarhus University Hospital have taken an important step towards a better understanding of the disease. Their research indicates that Parkinson’s disease may begin in the gastrointestinal tract and spread through the vagus nerve to the brain.
“We have conducted a registry study of almost 15,000 patients who have had the vagus nerve in their stomach severed. Between approximately 1970-1995 this procedure was a very common method of ulcer treatment. If it really is correct that Parkinson’s starts in the gut and spreads through the vagus nerve, then these vagotomy patients should naturally be protected against developing Parkinson’s disease,” explains postdoc at Aarhus University Elisabeth Svensson on the hypothesis behind the study.
“Our study shows that patients who have had the the entire vagus nerve severed were protected against Parkinson’s disease. Their risk was halved after 20 years. However, patients who had only had a small part of the vagus nerve severed where not protected. This also fits the hypothesis that the disease process is strongly dependent on a fully or partially intact vagus nerve to be able to reach and affect the brain,” she says.
The research was recently published in the journal “Annals of Neurology”.
Source: Aarhaus University
A digital map of the ageing brain could aid the diagnosis of Alzheimer’s disease and other neurodegenerative disorders in older people, a study suggests.
The atlas created using images from MRI scans of older people could aid diagnosis by comparing the patients’ scans with a detailed map of the healthy ageing brain.
Most existing MRI atlases are based on the brains of young and middle-aged people, which don’t reflect the normal changes that take place in the brain as we age, the team says. Researchers at the University of Edinburgh constructed a detailed atlas of the human brain using MRI scans from more than 130 healthy people aged 60 or over.
The team used their atlas to study brain scans taken of normal older subjects and those who had been diagnosed with Alzheimer’s disease. The atlas was able to pinpoint changes in patients’ brain structure that can be an underlying sign of the condition, researchers say.
The study is published in the journal PLOS ONE.
Dr David Alexander Dickie, of The University of Edinburgh’s Brain Research Imaging Centre and SINAPSE, who was first author of the study, said: “We’re absolutely delighted with these preliminary results and that our brain MRI atlases may be used to support earlier diagnoses of diseases such as Alzheimer’s. Earlier diagnoses are currently our strongest defence against these devastating diseases and, while our work is preliminary and ongoing, digital brain atlases are likely to be at the core of this defence.”
Source: University of Edinburgh
‘Seeding’ property provides new focus for treatment to delay progression of disorder
By identifying in spinal fluid how the characteristic mutant proteins of Huntington’s disease spread from cell to cell, researchers have created a new method to quickly and accurately track the presence and proliferation of these neuron-damaging compounds — a discovery that may accelerate the development of new drugs to treat this incurable disease.
The researchers added that the cell-to-cell “seeding” property of these mutant proteins seems to be a critical part of the disease’s progression. Their findings also advance a new drug-discovery approach: stopping the cellular transfer of the seeding compounds. Study results appear online in the journal “Molecular Psychiatry”.