Even hearing the phrase “Huntington’s disease” will make a room suddenly somber. So the joy that accompanied a recent announcement of results of an experimental gene therapy for the deadly diseases signaled an unfamiliar sense of hope.

In a small clinical trial, brain injections of a virus that codes for a tiny segment of RNA may have prevented the formation of the rogue proteins that make Huntington’s so devastating. The early results, announced September 24 in a news release, show that over three years, the treatment slowed Huntington’s progression by up to 75 percent. While not a cure, the treatment could potentially give people living with Huntington’s disease, who might otherwise face early disability and death, the gift of many more years of life.

The International Advisory Committee on Clinical Trials led a multinational panel updating the McDonald criteria, adding the optic nerve as a fifth anatomical location and allowing specific magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) markers to support diagnosis without mandatory dissemination in time in defined scenarios.

Multiple sclerosis diagnosis has long required proof that lesions occur in different places and at different times, with MRI and CSF biomarkers gradually shortening time to treatment.

Previous revisions improved sensitivity and specificity across ages and regions, yet misdiagnosis risk still persists, especially with overlapping conditions and when access to specialized tests is limited.

A new study led by the Icahn School of Medicine at Mount Sinai offers one of the most comprehensive views yet of how brain cells interact in Alzheimer’s disease, mapping protein networks that reveal communication failures and point to new therapeutic opportunities.

Published online in Cell, the study analyzed protein activity in brain tissue from nearly 200 individuals.

The researchers discovered that disruptions in communication between neurons and supporting brain cells called glia—specifically astrocytes and microglia—are closely linked to the progression of Alzheimer’s disease. One protein in particular, called AHNAK, was identified as a top driver of these harmful interactions.

Schizophrenia is a chronic mental health disorder characterized by hallucinations, delusions, disorganized thinking and atypical movement or speech patterns. This psychiatric condition can be highly debilitating, and diagnosed individuals can report markedly different experiences.

Understanding the neurobiological basis of schizophrenia could be highly valuable, as it could inform the development of new interventions to reduce the risk of its emergence or treat its symptoms. The results of many neuroimaging studies carried out so far, however, were inconsistent or inconclusive, failing to clearly delineate the processes and brain regions implicated in its clinical expression.

In a recent paper published in Nature Mental Health, researchers at Taipei Medical University analyzed meta-analyses summarizing the most consistent findings of schizophrenia-related neuroimaging studies. Drawing on the results of this analysis, they developed a new theoretical model that delineates characteristic brain alterations linked to the psychiatric disorder.