Novel potential Huntington's treatments
Written By : Isra Zaman
Medically Reviewed By : Dr. Kamal Kant Kohli
Published On 2022-08-31 03:30 GMT | Update On 2022-08-31 09:05 GMT
Advertisement
The two populations of glia found in the brain, oligodendrocytes and astrocytes, are dysfunctional in Huntington's disease and may be the primary cause of much of the neuronal pathology observed in the condition, according to research from the University of Rochester Medical Center.
Glia cells play a critical role in maintaining the health of neurons and facilitating the chemical signaling between nerve cells. In Huntington's, glia are unable to perform these functions, leading to a breakdown in communication between neurons and, over time, cell death.
The new study focuses on oligodendrocytes and identifies how the suppression of a specific transcription gene called Tcf7L2 triggers a series of changes that impair the function of oligodendrocyte progenitor cells (OPCs). These cells constantly resupply the brain with oligodendrocytes, which, in turn, refresh the myelin insulation that helps signals travel in the brain more crisply. In Huntington's, OPCs are not able to meet demand, leading to deficient myelination in the brain, which can be observed in Huntington's patients in the form of white matter atrophy. When the researchers overexpressed Tcf7l2 in mice with the Huntington's disease mutation, their OPCs recovered and restored the myelin that had been lost to the disease.
Ref:
Steve Goldman,A TCF7L2-reponsive suppression of both homeostatic and compensatory remyelination in Huntington disease mice,Cell Reports
Our comments section is governed by our Comments Policy . By posting comments at Medical Dialogues you automatically agree with our Comments Policy , Terms And Conditions and Privacy Policy .
Disclaimer: This website is primarily for healthcare professionals. The content here does not replace medical advice and should not be used as medical, diagnostic, endorsement, treatment, or prescription advice. Medical science evolves rapidly, and we strive to keep our information current. If you find any discrepancies, please contact us at corrections@medicaldialogues.in. Read our Correction Policy here. Nothing here should be used as a substitute for medical advice, diagnosis, or treatment. We do not endorse any healthcare advice that contradicts a physician's guidance. Use of this site is subject to our Terms of Use, Privacy Policy, and Advertisement Policy. For more details, read our Full Disclaimer here.
NOTE: Join us in combating medical misinformation. If you encounter a questionable health, medical, or medical education claim, email us at factcheck@medicaldialogues.in for evaluation.