Robert M. Friedlander, MD, MA

Chairman of the University of Pittsburgh Department of Neurological Surgery and co-director of the UPMC Neurological Institute

Dr. Friedlander's research will focus on synthesis of melatonin in the brain and if the natural decline in melatonin synthesis with age contributes to age-related neurodegeneration.  A breakthrough in this regard would lead to the establishment of a mouse model of age-related neurodegeneration with a future goal to use this model to identify new strategies for preventing neuro-degenerative diseases, such as dementia.

The Scientist Behind the Mission

Dr. Friedlander’s major research interests lie in the study of the mechanistic pathways of the caspase apoptosis gene family (cell death). His work includes the evaluation of treatment strategies for neurodegenerative diseases (Huntington’s and ALS), stroke, brain trauma, and spinal cord injury through the modulation of the caspase-family apoptotic pathways. You can read more about Dr. Friedlander's research and background in his University of Pittsburgh's Biography.

"Dementia robs people from their mind and what are we without our thoughts, what are we without being able to talk? All of these issues, are what we are trying to address."

- Dr. Robert Friedlander

Explore Friedlander's Dementia Research

Neurodegeneration and aging are linked, with most neurodegenerative diseases striking later in life.  However, the mechanisms by which neurons become vulnerable as they age are unknown.  Melatonin, a neuroprotectant when exogenously administered, is produced by the pineal gland for secretion, as well as by neurons and other cells for intracellular functions.  Melatonin-mediated cellular protection occurs by at least three distinct but complementary mechanisms.  Melatonin is a potent free radical scavenger, stimulates transcription and activity of antioxidant enzymes, and inhibits mitochondrial activation of caspase cell death pathways.  Therefore, age-related and disease-associated reduction of melatonin production likely increases cellular vulnerability resulting in age-related degenerative processes.  A significant gap exists in the availability of a valid in vivo tool to model age-related cellular vulnerability. The goal of this project is to develop and validate an in vivo a model of melatonin-depletion-mediated degeneration as a proxy ageing model.

Future Potential for this Project

This project will increase our understanding of aging mechanisms, including the effect of melatonin loss on neural function.  Since melatonin is widely used with few adverse effects, the ability of exogenous melatonin supplementation to inhibit the markers of aging would have significant potential for future development.  In addition, a developed mouse model will be validated as a resource for aging research resource, enhancing research across the geroscience field.