An Academia Sinica research team has uncovered via a mouse model the secrets of the formation of frontotemporal lobar degeneration (FTLD) , a brain disorder that causes dementia and for which there is currently no treatment, a researcher said Friday. Tsai Kuen-jer, an assistant professor at National Cheng Kung University's Graduate Institute of Clinical Medicine who took part in the research, touted the finding as a major breakthrough in the study of the neurodegenerative disease. Using the model will bring scientists closer to developing and creating efficient drugs or therapies to treat FTLD patients, Tsai said. According to Academia Sinica, Taiwan's highest academic research institute, FTLD is associated with atrophy in the frontal and temporal lobes of the brain that can lead to memory loss, impairment of language ability and sometimes motor neuron disease. It is one of the common causes of various kinds of dementia, including Alzheimer's disease. The research team, led by Academician Che-Kun James Shen at the the Institute of Molecular Biology, found an abnormal level of a type of cellular protein known as TAR DNA binding protein 43 (TDP-43) in the brains of FTLD sufferers. The protein, which is capable of affecting neural cell activity, should exist in the nucleus of a cell but is found at an increased levels in the cell plasma of people with FTLD, Tsai said. In the study, the researchers genetically engineered mice with increased levels of TDP-43 in the forebrain. They discovered that the mice exhibited symptoms that mimic FTLD. 'The finding that increased levels of TDP-43 protein in the forebrain are sufficient to cause FTLD and possibly other neurodegenerative diseases yields a new avenue for future studies of FTLD,' said the institute in a statement. It pointed out that Shen's research team has already started to test a few drugs with potential for treating FTLD and that a collaboration project with an Australia-based laboratory has also been established to conduct drug screening. The results of the research paper, titled 'Elevated Expression of TDP-43 in the Forebrain of Mice is Sufficient to Cause Neurological and Pathological Phenotypes Mimicking FTLD-U, ' were published July 27 in the peer-reviewed Journal of Experimental Medicine. 