Glia affected by Huntington’s disease respond by tuning down synapse genes, which has a protective effect.

This process of adjustment, a result of the brain’s plasticity, or its ability to change or reorganize neural networks, occurs in neurodegenerative conditions such as Alzheimer’s, Parkinson’s and Huntington’s disease (HD). As the conditions progress, many genes change the way they are normally expressed, turning some genes up and others down. The challenge for researchers like Dr. Juan Botas who studies HD, has been to determine which of the gene expression changes are involved in causing the disease and which ones help mitigate the damage, as this may be critical for designing effective therapeutic interventions.

In his lab at Baylor College of Medicine, Botas and his colleagues look to understand what causes the loss of communication or synapses between neurons in HD. Up until now, research has focused on neurons because the normal huntingtin gene, whose mutation causes the condition, contributes to maintaining healthy neuronal communication. In the current work, the researchers looked into synapses loss in HD from a different perspective.

Focusing on glia to understand Huntington’s disease

The mutated huntingtin gene is not only present in neurons, but in all the cells in the body, opening the possibility that other cell types also could be involved in the condition.

«In this study we focused on glia cells, which are a type of brain cell that is just as important as neurons to neuronal communication,» said Botas, professor of molecular and human genetics and of molecular and cellular biology at Baylor and a member of the Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital.

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Materials provided by Baylor College of Medicine. Original written by Ana Maria Rodriguez, Ph.D.. Note: Content may be edited for style and length.