Teresa Gomez-Isla, MD, PhD is the Anne B. Young Chair of Neurodegenerative Disease and Professor of Neurology at Harvard Medical School. She is the Chief of the Memory Division in the Neurology Department at Massachusetts General Hospital and the Director of the Dementia Fellowship Training Program. She also serves as Associate Director of the Massachusetts Alzheimer Disease Research Center and Principal Investigator of an Alzheimer’s Research Laboratory at the MassGeneral Institute for Neurodegenerative Disease. She obtained her MD at the University Complutense of Madrid in 1989 and her PhD at the University Autonoma of Madrid in 1995, then completed her residency in Neurology at Hospital Doce de Octubre in Madrid in 1994 and her fellowship in Dementia at Massachusetts General Hospital in 1997. She served as Director of the Memory Disorders Units at Clinica Universitaria of Navarre in Pamplona (Spain) and Hospital Santa Cruz y San Pablo in Barcelona (Spain) before moving to Mass General in 2009.

Dr. Gomez-Isla’s early work in 1995 demonstrated the underlying brain changes that mark the transition between normal aging and earliest clinical symptoms of Alzheimer’s disease, and the clinical and neuropathological impact of ApoE4, the main genetic risk factor identified so far in late onset Alzheimer’s disease. She also generated and characterized novel transgenic mouse models mimicking Alzheimer’s disease and related disorders that allowed to investigate new therapeutic strategies to halt tangle deposition and neuronal loss. More recently, she has conducted key validation studies of multiple novel tau Positron Emission Tomography tracers that have helped guiding the correct interpretation of in vivo neuroimaging biomarker studies in patients with Alzheimer’s disease and related disorders. Dr. Gomez-Isla is now focused, among others, on the study of brains from individuals who display robust amounts of Alzheimer’s pathology at autopsy but never developed symptoms of the disease during life. She has discovered that in these unique ‘resilient’ brains, as opposed to typically demented Alzheimer’s brains, there is reduced accumulation of soluble tau species in the synaptic compartment, little inflammatory changes, and decreased glia-mediated engulfment of synapses despite robust accumulation of plaques and tangles. These findings have potential implications for individual risk assessment and the search for novel therapeutic interventions directed to preserve cognition in the setting of classic Alzheimer disease neuropathologic changes.

She is a Spanish Society of Neurology Alzheimer award winner, Spanish Alzheimer Association (Cuenca) award winner, and Ernesto Gonzalez award winner (for outstanding services to Hispanic community). She serves in the National Alzheimer’s Coordinating Center (NACC) Clinical Task Force and the World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for the biological treatment of Alzheimer’s disease and other dementias. She has contributed to train multiple generations of young clinicians and scientist in the Alzheimer’s field. Her main goals are to provide the best possible clinical care to patients with dementia, fight inequality in access to clinical care and research opportunities for underserved communities, implement novel therapeutic strategies for patients with dementia, and train and inspire the future generation of clinician-scientists in the field of Alzheimer’s disease and related disorders.