This study shows for the first time that abnormal TDP-43 protein causes loss of life of astrocytes. The researchers, however, found that the damaged astrocytes weren’t directly toxic to engine neurons. Better understanding the part of astrocytes could help to see research into remedies for MND. Professor Siddharthan Chandran, of the University of Edinburgh, said: ‘Motor neurone disease is a devastating and eventually fatal condition, for which there is no treatment or effective treatment. It is not a issue of looking solely at motor neurons just, but also the cells that surround them, to understand why engine neurons die. Our purpose is to find ways to slow down progression of this devastating disease and ultimately develop a treat.’ Related StoriesGriffith University uncovers initial 3-D image of protein linked to cancers spreadNew Global Energy and International Sustainability Group consent to manufacture, distribute MoringaUP Protein BarsUnderstanding how schizophrenia affects workings of the brain These findings, published in the journal Proceedings of the National Academy of Sciences., are significant as they present that different mechanisms are at work in different types of MND.We hypothesize that TEX11 mutations disturb the function and development of the synaptonemal complex, causing main disruption of pachytene synapsis and anaphase spindle checkpoints; the disruption, in turn, triggers meiotic arrest, spermatocyte apoptosis, and azoospermia. This model is supported by computational framework analysis and immunostaining results in sufferers with azoospermia, meiotic arrest, and TEX11 mutations; in these patients, we did not detect TEX11 expression and noted massive lack of late spermatocytes and round and elongated spermatids. Notably, wild-type TEX11 expression differs substantially among several mammalian species with normal sperm concentrations .