About Alberto Serrano Pozo, MD, PhD

Dr. Serrano-Pozo is originally from Málaga, Spain. He received his MD in 2001 at the University of Málaga School of Medicine and completed his neurology residency in 2006 at the University Hospital Virgen del Rocío in Seville (Spain), followed by a 2-year research and behavioral neurology fellowship at the same institution. He first joined Dr. Bradley Hyman’s lab at MGH as a research fellow in 2008, where he investigated clinic-pathological correlations of Alzheimer’s dementia using brain specimens from the Massachusetts Alzheimer’s Disease Research Center brain bank, as well as the National Alzheimer’s Coordinating Center (NACC) database. His publications during this period resulted in Dr. Serrano-Pozo obtaining his PhD at the University of Seville in 2013. Next, he pursued a US neurology residency, which he completed at the University of Iowa in 2017 as Chief Resident. He then returned to MGH to complete a Clinical Dementia fellowship and pursue his career as clinician-scientist in the field of Alzheimer's disease and related dementias. 

Clinical Interests:




Mass General Neurology
55 Fruit St.
Boston, MA 02114
Phone: 855-644-6387

Medical Education

  • MD, University of Malaga-Spain
  • Residency, University Hospital Spain
  • Residency, University of Iowa Hospital & Clinics
  • Fellowship, Massachusetts General Hospital

American Board Certifications

  • Neurology, American Board of Psychiatry and Neurology

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I am a clinician-scientist neurologist with interest in Alzheimer’s disease and other neurodegenerative dementias. My research focuses on trying to explain how the amyloid plaques and neurofibrillary tangles accumulate in the brain of Alzheimer’s disease patients and how they lead to dementia. I first approached this question by studying postmortem brain specimens from Alzheimer’s disease patients and healthy individuals under the microscope. The findings of my unbiased quantitative analyses supported an important role of glial (non-neuronal) cells, specifically astrocytes and microglial cells. These cells clearly react to plaques and tangles, but the consequences of this response remain largely unknown. Therefore, I became interested in understanding the underlying mechanisms of glial responses and their effects on Alzheimer’s disease development and progression.


  • Selected publications:

    • Qian J, Betensky RA, Hyman BT, Serrano-Pozo A. Association of APOE genotype with heterogeneity of cognitive decline rate in Alzheimer’s disease. Neurology 2021 (in press).
    • Escartin C*, Galea E*, Lakatos A**, O’Callaghan J**, Petzold G**, Serrano-Pozo A**, et al. Reactive astrocyte nomenclature, definitions, and future directions. Nat Neurosci 2021; 24(5): 312-25.
    • Noori A, Mezlini AM, Hyman BT, Serrano-Pozo A*, Das S*. Systematic review and meta-analysis of human transcriptomics reveals neuroinflammation, deficient energy metabolism, and proteostasis failure across neurodegeneration. Neurobiol Dis 2021; 149: 105225.
    • Serrano-Pozo A, Das S, Hyman BT. APOE and Alzheimer’s disease: advances in genetics, pathophysiology, and therapeutic approaches. Lancet Neurol 2021; 20(1): 68-80.
    • Das S*, Li Z*, Noori A, Hyman BT, Serrano-Pozo A. Meta-analysis of mouse transcriptomic studies supports a context-dependent astrocyte reaction in acute CNS injury versus neurodegeneration. J Neuroinflammation 2020; 17(1): 227.
    • Gui Y, Marks JD, Das S, Hyman BT, Serrano-Pozo A. Characterization of the 18 kDa translocator protein (TSPO) in post-mortem normal and Alzheimer’s brains. Brain Pathol 2020; 30(1): 151-164.

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