Mounting evidence suggests that age-related cognitive decline is caused not by nerve cell death, as it is in Alzheimer’s disease, but from a disruption in synapses, the structures that allow a nerve cell to transmit a signal to other nerve cells. Demonstrating these synaptic disruptions in the prefrontal cortex of the brain, and linking such disruptions to synaptic health, has been challenging for scientists—until now.
Research in Mark Baxter’s laboratory, the Glickenhaus Laboratory of Neuropsychology, focuses on the neural systems underlying memory and other higher cognitive functions, and understanding how disturbances in these systems impair cognitive function in brain disorders. Our general approach is to study the effects on behavior of specific manipulations of neural circuits in animal models, to gain insight into how similar disruptions in human disease may be responsible for cognitive impairment.
For most of us the word brain is synonymous with nerve cells or neurons. All of us are well familiar with the notion of the brain as a mega-computer where billions of neurons govern our life, from simplest tasks to the rare moments of discoveries. It may appear surprising to hear that the function of brain and neurons would not be possible without cells that do not participate in our thinking directly. Instead, these cells, that are called microglia, function as watchdogs of neuron’s functionality and health and remove neurons that stop acting properly.