The brain’s support cells show defective development in Huntington’s disease

Typically the neurological disorder Huntington’s disease causes behavioural and electric motor changes, which among other things are a effect of dysfunctional maturation or formation of glial tissue, the brain’s support tissue, researchers from the University or college of Copenhagen demonstrate in a new study centered on mice trials. Typically the researchers’ long-term goal is to be able to use the research results to develop a treatment for Huntington’s disease using glial cells.

The brain’s support cells, the apparent glial cells, play a primary role in the development of the genetic brain disorder Huntington’s disease, for which there is at present no treatment. In a new study, an international group of researchers from the Faculty of Well being and Medical Sciences at the University of Copenhagen, among others, has now mapped important, hitherto unidentified mechanisms in glial tissues in a brain struggling from Huntington’s disease. The particular new research results have been published in the journal Cell Stem Cellular.

‘In the study we show that glial cellular maturation is severely reduced in patients with Huntington’s disease, and this is a major contributor to the abnormalities we see in the brain. This contributes to behavioural changes as well as to changes in engine function. The failure of glial maturation causes many of these symptoms, because diseased glial cells are not able to support normal neuronal and synaptic function; this means that the communication between neurons is impaired, claims the last author of the study, Professor Sam Goldman from the Middle for Neuroscience at the University of Copenhagen and the Center for Translational Neuromedicine at University of Rochester.

Huntington’s disease is the result of a veränderung in a gene — the Huntingtin gene — which codes for a protein that when mutated causes the disease. Amongst other things, Huntington’s disease contributes to personality changes and a loss in engine coordination. There is presently no treatment that can cure or even slow the condition; at best, physicians can only offer medicines that can alleviate some of its symptoms. The entire goal of Steve Goldman and his research group is to find a meaningful, disease-modifying treatment for the disease.

They have been researching glial tissues and degenerative diseases in the brain, including Huntington’s disease, for a quantity of years, and in this study they arranged out to figure out what happens to glial cells at the molecular level in the Huntington’s disease brain. To do so the researchers studied mice into which they had transplanted human glial progenitor tissues containing the Huntington gene. These glial progenitor tissues are precursors to adult glial cells, and were derived from pluripotent originate cells, using methods that the researchers developed for producing glial cells from stem cells.

Common Characteristic: Dysfunctional Glial Cells These kinds of mice with human glia enabled the researchers to examine the development of Huntington disease-derived glial cells. Typically the researchers found that the growth of the glia was delayed and imperfect. Between other things, this generated dysfunctional astrocytes, the most prevalent form of glia in the brain, which among other things regulate the communication between neurons. This poor glial maturation also generated a lack of myelin, the insulating fat that encircle the nerve pathways in mental performance, and which normally allows and speeds nerve organs communication. The result was a failure of the brain’s white matter in these humanized mouse types of Huntington disease, with their consequent effects on conduct and motor skills. Goldman argues that glial tissue are important in relationship with Huntington’s disease, but also appear to play a primary role in several other neurodegenerative and neuropsychiatric diseases, such as schizophrenia.

‘This failure of glial cell maturation appears to be a common factor of diseases that require behavioural abnormalities and psychotic thinking. The unsuccessful glial cell maturation we found in Huntington’s disease is much like what we noticed in one in our earlier studies, where we analyzed the role of glial cells in schizophrenia. In the same time, our study stresses the possible of glial cell remedy as a possible treatment for Huntington’s disease and other similar neurodegenerative diseases’, Goldman explains.

Goldman and his colleagues have formerly worked with glial cellular transplantation, as described in a study from 2016. Here the researchers experienced transplanted healthy glial tissues to mice suffering from Huntington’s disease. This extented the life expectancy of the mice and relieved the symptoms of the condition. And one of the next steps for Goldman and his research team is to conduct medical trials involving transplantation of healthy glial cells to patients with Huntington’s disease. They hope to be able to launch these trials within the next few years.

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