In a recent study published in the journal Aging, a team of UF neuroscientists examined a mechanism associated with disruption of synaptic plasticity and cognition in neurological and psychiatric diseases and aging. The investigators explored the role of subunit contribution of N-methyl-D-aspartate (NMDA) receptor hypofunction and redox sensitivity of hippocampal synaptic transmission during aging. Recent work has identified a redox-signaling as a mechanism linking decreased NMDA receptor function with cognitive deficits of Alzheimer’s disease, depression, schizophrenia and aging.
The results of the new study, led by Ashok Kumar, Ph.D., associate professor of neuroscience; Jeffrey Thinschmidt, scientific research manager of pharmacology and therapeutics; and Thomas Foster, Ph.D., Evelyn F. McKnight chair for research on cognitive aging and memory; indicate that activity-dependent NMDA receptor synaptic plasticity is suppressed by redox-mediated inhibition of Ca2+/calmodulin-dependent protein kinase II (CaMKII) activation during aging. The redox regulation of NMDA receptors represents a suppression of a metaplasticity mechanism, which can disrupt synaptic plasticity and cognition linked with neurological and psychiatric diseases as well as aging.