Cross-species transcriptomic analysis and high-throughput behavioral assays in a Drosophila model of Huntington's disease show that downregulation of glial genes involved in synaptic function compensates for disease-related excitotoxicity.

Uninterrupted CAG repeat length determines onset age in Huntington's disease, and therefore, base editing strategies to generate CAA interruption offer new therapeutic opportunities as they diminish the disease-causing mutation.

Progression of Huntington's disease can be slowed by altering dopamine signalling through the Dopamine 1 receptor - Histamine 3 receptor heteromer.

In a premanifest mouse model of Huntington's disease at a stage very far from disease onset, significant network and behavior dysregulation was found, being rebalanced by treatment with metformin.

A novel BAC226Q mouse recapitulating robust, age-dependent, progressive Huntington’s disease (HD)-like phenotypes will be a valuable tool for studying disease mechanisms, identifying biomarkers, and testing gene-targeting therapeutic approaches for HD.

In mouse models of Huntington's disease, the subthalamic nucleus, which suppresses movements, also exhibits impaired glutamate homeostasis, NMDA receptor-dependent mitochondrial oxidant stress, firing disruption, and 30% neuronal loss.

In a model of human neurulation (neuruloids), YAP is deferentially regulated across ecotodermal lineages, where it contributes to their differentiation and structural organization, and is hyper-active upon HD mutation, contributing to an HD-signature phenotype.

A cell-surface receptor called Gpr52 is able to lower the levels of the disease-causing protein mutant huntingtin and suppress its toxicity when knocked-down, making this receptor a promising drug target in Huntington's disease.

Genetic knockout of Hdac2 modifies molecular and cellular phenotypes in Huntington’s disease mice and has a prominent transcriptional regulatory role in adult medium spiny neurons.

mHTT delivery in key cortical and subcortical brain regions leads to hallmark mHTT aggregate formation, gray and white matter degenerative changes, along with motor and cognitive decline in a new macaque model of Huntington's disease.