Monthly Archives: July 2015

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:


Call overview:

Stage 1 proposals:

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