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.

Impaired GABAergic and glutamatergic synaptic function and loss of interneurons in the amygdala, hippocampus, and cerebellum cause characteristic disease symptoms in a mouse model juvenile neuronal ceroid lipofuscinosis.

Experiments on flies suggest that a gain-of-function mechanism in a protein called CSPɑ contributes to the progressive brain disease CLN4.

Boosting the function of translation factor eIF2B by chronic small molecule administration prevents pathology in a neurodegenerative model of Vanishing White Matter disease characterized by a maladaptive stress response.

Globotriaosylcermide directly impacts neuronal integrity and ion channel function as potential mechanism underlying small fiber pathology in Fabry disease.

GDC-0810 is a novel, orally bioavailable SERD that exhibits robust pre-clinical activity in models of ER+ breast cancer, including models of tamoxifen resistance, and those that express the ERα mutations, ER.Y537S and ER.D538G.

Human neuroimaging and machine learning reveals a generalizable relationship between brain connectivity and working memory ability across healthy populations and distinct psychiatric diagnoses.

Genetically restoring Mecp2 expression only in GABAergic neurons in a mouse model of Rett syndrome improves inhibitory signaling, extends lifespan and rescues most but not all behavioral deficits.

By binding to Fc gamma receptor IIb, amyloid beta induces a series of phosphorylation events that mediate the damaging effects of hyperphosphorylated tau proteins in Alzheimer's disease.