Skip to main content

Micro-RNA Role in Alzheimer's Disease

Proteins are the molecular machines of the cell. They transport materials, cleave products or transmit signals -- and for a long time, they have been a main focus of attention in molecular biology research. In the last two decades, however, another class of critically important molecules has emerged: small RNA molecules, including micro-RNAs. It is now well established that micro-RNAs play a key role in the regulation of cell function."A micro-RNA regulates the production of an estimated 300-400 proteins.

This class of molecules can be regarded as a switch that coordinates the transition of cells from one state to another," explains Prof. Dr. André Fischer, scientist at the German Center for Neurodegenerative Diseases (DZNE) and Speaker of the DZNE site Göttingen. He and his team have identified a micro-RNA that regulates the learning processes and probably plays a central role in Alzheimer's disease. The researchers have shown that there is too much of a micro-RNA called "miRNA 34c" in mouse models of Alzheimer's disease, and decreasing the level of miRNA 34c in these mice can restore their learning ability. The scientists have identified a new target molecule that might be important for diagnosis and treatment of Alzheimer's disease. The studies were carried out in collaboration with scientists at the European Neuroscience Institute Göttingen, the Göttingen University, the DZNE site in Munich and researchers from Switzerland, USA and Brazil.

miRNA 34c was identified using a highly complex method called "massive parallel sequencing." With this technology, Fischer and his colleagues captured the complete RNA composition in the hippocampus -- the learning region of the brain -- and compared this with the RNA of the entire brain. They showed that miRNA 34c is enriched in the hippocampus, especially in during the time window of a few hours after a learning phase. "We suspect that the function of micro-RNA 34c is to switch off a whole range of gene products that are turned on in the learning process," Fischer said. Too much miRNA 34c would then lead to a blockade of learning -- which is exactly what was shown in subsequent experiments.

In old mice, which do not learn as easily as their younger counterparts, there was indeed too much miRNA 34c. The miRNA-34c level was also elevated in mice that are used as specific research models of Alzheimer's disease. These mice carry a genetic mutation that can cause Alzheimer's in humans and show disturbances of memory function. Moreover, miRNA 34c seems to not only play a role in mice. Fischer and his colleagues showed these levels are also elevated in the brains of Alzheimer's patients.

In further mouse experiments, the researchers showed that miRNA 34c is actually causally involved in the pathogenesis of Alzheimer's disease and memory disorders. An artificial increase of miRNA-34c level in normal mice results in memory impairment in the animals. Secondly, as Fischer and his colleagues have shown, lowering miRNA-34c levels can restore learning ability in mouse models of Alzheimer's disease and in older mice. "Neurodegenerative diseases like Alzheimer's are associated with many factors. We hope that with the identification of micro-RNA 34c, we have found an important mediator of pathogenesis," says Fischer. "Micro-RNA 34c would then be a good candidate for the development of drugs against Alzheimer's."

Athanasios Zovoilis, Hope Y Agbemenyah, Roberto C Agis-Balboa, Roman M Stilling,Dieter Edbauer, Pooja Rao, Laurent Farinelli, Ivanna Delalle, Andrea Schmitt, Peter Falkai, Sanaz Bahari-Javan, Susanne Burkhardt, Farahnaz Sananbenesi1 & Andre Fischer. Micro-RNA-34C is a novel target to treat dementias. EMBO Journal, 2011.327

Comments

Popular posts from this blog

Neuronal Switch to Prevent Neurodegenerative Diseases

Scientists at Northwestern University report a surprising discovery that offers a possible new route for the treatment of neurodegenerative diseases. In a study of the transparent roundworm C. elegans, they found that a genetic switch in master neurons inhibits the proper functioning of protective cell stress responses, leading to the accumulation of misfolded and damaged proteins. Neurodegenerative diseases, ranging from Huntington's and Parkinson's to amyotrophic lateral sclerosis and Alzheimer's, are believed to stem from early events that lead to an accumulation of damaged proteins in cells. Yet all animals, including humans, have an ancient and very powerful mechanism for detecting and responding to such damage, known as the heat shock response. "Why are these diseases so widespread if our cells have ways to detect and prevent damaged proteins from accumulating?" said Richard I. Morimoto, who led the research together with postdoctoral colleague Veena Prah...

Dystonia Medical Research Foundation Honors Two Warren Men for Promoting Awareness of Debilitating Disease

Jason Dunn and Mike Delise recently returned from the Children & Family Dystonia Symposium in Chicago, where they were presented with Star Awards. The Dystonia Medical Research Foundation (DMRF) recognized Dunn and Delise for their efforts to promote greater public awareness of dystonia, a neurological disease. "I think this is probably the only time in my life that I am speechless," says Dunn. "I wasn't expecting this award at all." "Bringing awareness and donations to the Dystonia Medical Research Foundation is the single most important thing we can do--this is how a cure will be found," says Delise. "The people who deserve this award are all the people who have dystonia who bring awareness every minute of their life. Jason is my hero and to be able to help your hero is a thrill for me." Dunn began exhibiting unusual postures and an awkward gait at age 6. While most children this age are mastering their abilities to run, jump, and so...

Human Brain Doesn't Stop Developing at Adolescence

Source: University of Alberta Faculty of Medicine & Dentistry. The human brain doesn't stop developing at adolescence, but continues well into our 20s, demonstrates recent research from the Faculty of Medicine & Dentistry at the University of Alberta.  It has been a long-held belief in medical communities that the human brain stopped developing in adolescence. But now there is evidence that this is in fact not the case, thanks to medical research conducted in the Department of Biomedical Engineering by researcher Christian Beaulieu, an Alberta Innovates -- Health Solutions scientist, and by his PhD student at the time, Catherine Lebel. Lebel recently moved to the United States to work at UCLA, where she is a post-doctoral fellow working with an expert in brain-imaging research. "This is the first long-range study, using a type of imaging that looks at brain wiring, to show that in the white matter there are still structural changes happening during young adult...