John Morrison
Academic Editor

John H. Morrison


Summary

Dean of Basic Sciences and the Graduate School of Biological Sciences and Professor of Neuroscience at Mount Sinai School of Medicine. Former President of the Cajal Club and The Harvey Society, and current member of Council for the Society for Neuroscience. Merit Award recipient from NIH.

Dr. Morrison is also the Willard T.C. Johnson Professor of Geriatrics and Palliative Medicine in Neurobiology of Aging, and Professor in the Friedman Brain Institute.

Cell Biology Cognitive Disorders Geriatrics Neuroscience Palliative Care Psychiatry & Psychology

Institution affiliations

Work details

Dean and Professor

Mount Sinai School of Medicine
Department of Neuroscience
We work on synaptic plasticity, the aging brain, and the synaptic basis of age-related cognitive decline. We are particularly interested in the distinction between Alzheimer's disease (AD) and the more modest disruption of memory often referred to as age-associated cognitive impairment or mild cognitive impairment (MCI) that often occurs in the context of normal aging. While age-associated cognitive impairment represents a major health problem on its own that must be solved, preventing the transition from MCI to AD is a related goal of enormous importance given the rising threat and cost of AD to western society. In order to achieve either goal, we need to understand the cellular, synaptic, and molecular basis of the earliest age-related alterations that lead to cognitive decline and how these events relate to the complex physiology of aging, such as the aging of endocrine systems that affect the brain, or the interactions between stress and aging. For example, in AD, the cortical neurons that provide the complex connections that mediate cognition degenerate, leading to the catastrophic loss of cognitive function evident in dementia. Unlike AD, significant neuron death does not occur in normal aging and thus does not appear to be the cause of the initial stages of age-associated cognitive impairment. While these circuits do not die in normal aging, we have shown that they are vulnerable to sub-lethal age-related alterations in structure, synaptic integrity, and molecular processing at the synapse, all of which impair cognitive function in well-characterized animal models. In addition, while synapse loss occurs in aging, all synapses are not equally vulnerable and all regions do not age the same way. Our recent data on prefrontal cortex show that there is a selective loss of the class of synapses that is most plastic and likely to play a critical role in the cognitive processes mediated by prefrontal cortex, yet the age-related synaptic alterations in hippocampus are quite different, with minimal synapse loss. Biochemical alterations of the synapse, such as shifts in distribution or abundance of key neurotransmitter receptors, may also contribute to memory impairment, particularly in hippocampus.