Neuroinflammation and Cognition

Increased human longevity has magnified the negative impact that aging can have on cognitive performance. The number of individuals 65 years or older will increase exponentially over the next several decades and age-related cognitive impairment is expected to have a detrimental impact on individuals, their families, and society. An early sign of age-related cognitive decline in humans and rodent models is impaired executive function and spatial memory performance. Synaptic plasticity in the mammalian central nervous system has been the subject of intense investigation and is regarded as a principal candidate for cellular mechanisms involved in learning and memory. Senescent physiology, including altered synaptic plasticity and cell excitability, is thought to contribute to the decline in cognitive function associated with aging and age-associated neurodegenerative diseases. Neuroinflammation is a common feature of virtually every central nervous system disease, and is being increasingly recognized as a potential mediator of cognitive impairments. The impact of age on neuroinflammatory responses--including glial activation, increased production of proinflammatory cytokines, and aberrant neuronal signaling--could magnify the deterioration of the central nervous system microenvironment in disease, and may contribute to accelerated cognitive impairment. However, a clear mechanistic understanding of these interactions is lacking.

This Research Topic will focus on age-associated alterations in oxidative stress, neuroinflammation, and neurogenesis, and its influence on synaptic plasticity, cell excitability, and cognitive integrity. Special attention will be paid to the role of oxidative stress and inflammation in neurodegenerative diseases, and the impact this might have on cognition over the life span.