Glutamatergic regulation prevents hippocampal-dependent age-related cognitive decline through dendritic spine clustering.

ABSTRACT: The dementia of Alzheimer's disease (AD) results primarily from degeneration of neurons that furnish glutamatergic corticocortical connections that subserve cognition. Although neuron death is minimal in the absence of AD, age-related cognitive decline does occur in animals as well as humans, and it decreases quality of life for elderly people. Age-related cognitive decline has been linked to synapse loss and/or alterations of synaptic proteins that impair function in regions such as the hippocampus and prefrontal cortex. These synaptic alterations are likely reversible, such that maintenance of synaptic health in the face of aging is a critically important therapeutic goal. Here, we show that riluzole can protect against some of the synaptic alterations in hippocampus that are linked to a

SUBMITTER: Pereira AC 

PROVIDER: S-EPMC4284552 | biostudies-literature | 2014 Dec

REPOSITORIES: biostudies-literature