Robert Malinow, MD, PhD, professor of neurosciences at the University of California, San Diego School of Medicine, has been named the first recipient of the Shiley-Marcos Endowed Chair in Alzheimer’s Disease Research in Honor of Dr. Leon Thal. Malinow, a respected physician-scientist whose work focuses on the neurological connections at the foundation of memory and memory loss, was recognized at a reception in his honor hosted by Darlene Shiley at the La Jolla Country Club on November 12.

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Robert Malinow, MD, PhD, named first recipient of the Shiley-Marcos Endowed Chair in Alzheimer's Disease Research.
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Darlene Shiley and her husband, Donald Shiley, funded the chair in honor of her late mother, Dee Marcos. The chair was also named in honor of the late chair of neurosciences and director of the Shiley-Marcos Alzheimer’s Disease Research Center, Leon Thal, MD, a renowned Alzheimer’s disease researcher who died in a single-engine airplane crash in early 2007.
“We are delighted that Dr. Malinow accepted our invitation to join the UC San Diego Department of Neurosciences and serve as our first Shiley-Marcos Endowed Chair recipient,” said Doris Trauner, MD, interim chair of the department of neurosciences. “We are very excited about his past research accomplishments as well as the opportunity for him to make significant new contributions to Alzheimer’s disease research in the future.”
Malinow came to the UC San Diego School of Medicine in March 2008 from Cold Spring Harbor Laboratory, a private, non-profit research institution in New York, where he held the Alle Davis and Maxine Harrison Endowed Chair of Neurosciences since 1998. His research focuses on synaptic transmission and plasticity, learning and memory. He received his medical degree from New York University and his PhD degree from UC Berkeley. Malinow has received numerous awards including the MetLife Foundation Award for Medical Research and has been keynote speaker in several venues including the Einar Hille Memorial Lecture, KAC Elliot Lecture and Gordon Conference on Synaptic Transmission.
“For the past 20 years, I have studied the very basic properties of synapses – the connections between neurons in the brain – and how they change in strength when you learn something new or retrieve a memory,” said Malinow.
Because synapses and the underlying molecular signaling are critical to memory, Malinow and his research team study how exactly they work and what role synapses play in the memory loss associated with Alzheimer’s disease. They are looking at how beta amyloid – a protein fragment that may cause Alzheimer's – affects synapses and could weaken them, preventing memories to be formed.
“We believe beta amyloid taps into the normal processes used by synapses in order to modify their circuitry,” Malinow said. “Too much beta amyloid likely weakens synapses, preventing them from forming new memories and eventually leads to lost synapses.”
His second area of interest is depression and its relationship to synapses. Synapses in the part of the brain called the “disappointment center” are abnormally strong in depressed animals, according to Malinow, and this might offer clues to the cause and treatment of depression.
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Media Contact: Debra Kain, 619-543-6163, ddkain@ucsd.edu