Robert C. Malenka, M.D., Ph.D.

Pritzker Professor of Psychiatry and Behavioral Sciences
Director of the Pritzker Laboratory
Stanford University School of Medicine

Dr. Robert C. Malenka is the Pritzker Professor of Psychiatry and Behavioral Sciences, Director of the Pritzker Laboratory, and co-director of the Stanford Institute for Neuro-Innovation and Translational Neurosciences at the Stanford University School of Medicine.

Dr. Malenka is a world leader in elucidating the molecular mechanisms by which neural circuits are reorganized by experience. His many contributions over the last 25 years have laid the groundwork for a much more sophisticated understanding of the mechanisms by which neurons communicate and the adaptations in synaptic communication which underlie all forms of normal and pathological behavior. He has been at the forefront of helping to apply the knowledge gained from basic neuroscience research to the treatment and prevention of major neuropsychiatric disorders. He is an elected member of the Institute of Medicine of the National Academy of Sciences (2004) and an elected fellow of the American Academy of Arts and Sciences (2005) and the American Association for the Advancement of Science (2009). His public service includes serving on the National Advisory Council on Drug Abuse and as a councilor for the Society for Neuroscience. He is the co-author of the textbook Molecular Neuropharmacology: A Foundation for Clinical Neuroscience and has served on the editorial boards of many prominent journals, including Neuron, Trends in Neuroscience, Biological Psychiatry and the American Journal of Psychiatry.

Funded Research

Project Description Researchers Funding
Molecular mechanisms of synaptic plasticity in the hippocampus: A path to novel therapies

There is strong evidence suggesting that Alzheimer’s disease is caused in large part by the accumulation of a toxic protein termed A-beta (Aβ) in the brain. If scientists can understand in great molecular detail the very early steps of how Aβ accumulation impairs brain function, it will be possible to develop therapies that prevent these steps.  One of the earliest effects of toxic forms of Aβ is to impair the ability of the connections between nerve cells, termed synapses, to modify their own properties in response to changes in the patterns of brain activity.

2014
$100,000