Monthly Archives: December 2017

To mark the half-way point of the three-year projects funded in 2015 for the JPco-fuND call, the project coordinators of the 21 projects met for a two-day symposium in The Hague to learn about each other’s work, strengthen existing ties and build new relationships to further enhance research into neurodegenerative diseases. This meeting was a unique opportunity for each researcher to discover the wide variety and the cutting-edge level of the projects, raising new perspectives for all of them.

The researchers, whose projects focus on diseases ranging from Alzheimer’s and Parkinson’s diseases to rarer maladies such as Huntington’s disease, ALS, SCA3 and PolyQ, were invited to give brief seven-minute presentations on their work. The presentations were followed by lively Q&A sessions moderated by JPND representatives including Thomas Gasser, Myrra Vernooij-Dassen, Philippe Amouyel and Jesus de Pedro.

The scientific sessions were complemented with an informative seminar on data management and data sharing.  The seminar highlighted the importance—and the difficulties—of collecting, storing and sharing data. The second day featured a presentation of JPND’s most recent tools, the Experimental Models in Parkinson’s site, the Global Cohort Portal and the research funding database.

After each of the four scientific sessions, participants had the chance to network during coffee breaks and meals, as well as tour the poster presentations given by a young scientist from each consortium. “The role of JPND is to bring together scientists to encourage the cross-pollination of ideas and to favour new collaborations, allowing them to share the latest advancements in their fields and build relationships that will strengthen their research now and in the future,” said Philippe Amouyel, Chair of JPND.

Whilst several project consortia are already collaborating, the Symposium offered participants a host of networking opportunities, as well as a unique chance to get a glimpse of each other’s work and progress and encouraged researchers to further explore new ways to collaborate and connect.  As a result, the Symposium proved to be an enriching experience for all. The Final Symposium, where each project will report on the final results of their three years of work, is slated to take place in 2019.

For details on the JPco-fuND projects, click here.

To learn more about the progress of the JPco-fuND projects, read the presentation abstracts here.

Scientists have published a proof-of-concept study in the journal Neurobiology of Disease demonstrating that an antidepressant drug which has been on the market for more than 50 years could slow the progression of Parkinson’s.

The drug nortriptyline, which has been used to treat depression and nerve pain, stopped the growth of abnormal proteins that can build up in the brain and lead to the development of the disease.

Researchers began by examining previous patient data to see if individuals who were on antidepressants started a standard Parkinson’s therapy called levodopa later than those not taking the antidepressant. Levodopa increases levels of dopamine, a natural chemical in the body that sends signals to other nerve cells, which is usually significantly decreased in people with Parkinson’s. The medication also alleviates symptoms of the disease such as tremors and poor muscle control.

The researchers observed that people on tricyclic antidepressants did not need levodopa until much later, compared to patients not taking a tricyclic for depression.

Researchers then began testing rats with the tricyclic antidepressant nortriptyline and observed that it decreased the amount of alpha-synuclein, an abnormal protein that can build up in the brain and cause nerve cells to die. Alpha-synuclein buildup is a hallmark of Parkinson’s diease.

Finally, the scientists added nortriptyline to alpha-synuclein proteins in a test tube model and observed that the addition of the antidepressant caused the proteins to move and change shape more rapidly, preventing them from clumping together.

To further back up his research, he enlisted the help of his colleague and co-author Lisa Lapidus, who in previous studies had already detected whether certain compounds could bind to alpha-synuclein and stop it from accumulating.

Understanding how these proteins can clump together could point researchers in new directions and help them find other possible drugs that could potentially treat Parkinson’s.

Paper: “Nortriptyline inhibits aggregation and neurotoxicity of alpha-synuclein by enhancing reconfiguration of the monomeric form

Reprinted from materials provided by Michigan State University.