12 research outputs found
Inhibition of mitotic kinase Aurora suppresses Akt-1 activation and induces apoptotic cell death in all-trans retinoid acid-resistant acute promyelocytic leukemia cells
CaMKIIdelta overexpression in hypertrophy and heart failure: cellular consequences for excitation-contraction coupling
Do glia drive synaptic and cognitive impairment in disease?
Synaptic dysfunction is a hallmark of many neurodegenerative and psychiatric brain disorders, yet we know remarkably little about the mechanisms that underlie synaptic vulnerability. Although neuroinflammation and reactive gliosis are prominent in virtually every CNS disease, glia are largely viewed as passive responders to neuronal damage rather than drivers of synaptic dysfunction. This perspective is changing with the growing realization that glia actively signal with neurons and influence synaptic development, transmission, and plasticity through an array of secreted and contact-dependent signals. We propose that disruptions in neuron-glia signaling contribute to synaptic and cognitive impairment in disease. Illuminating the mechanisms by which glia influence synapse function may lead to the development of novel therapies and biomarkers for synaptic dysfunction
Concurrent SCI and TBI: Epidemiology, Shared Pathophysiology, Assessment, and Prognostication
Psychostimulants and Other Drugs Used in the Treatment of Attention-Deficit/Hyperactivity Disorder (ADHD)
The term “psychostimulants” (synonym stimulants) refers to a group of psychopharmacological agents whose predominant effect is the enhancement of cognitive and behavioral functions by stimulation of the central nervous system (CNS). In healthy humans, they relieve feelings of tiredness and languor, elevate mood, as well as improve concentration and performance. In animals, psychostimulants increase locomotor activity and are readily self-administered due to their powerful reinforcing properties
