Assistant Research Professor of Neurology, Institute for Academic Medicine
Assistant Research Member, Research Institute
Weill Cornell Medical College
Aaron D. Thome, Ph.D. grew up in Houston, Texas and completed his bachelor degree in Biomedical Science at Texas A&M University in College Station, Texas. Following this, he completed his doctorate work at the University of Alabama at Birmingham (UAB) under David G. Standaert, M.D., Ph.D., the John N. Whitaker Chair of Neurology at UAB. Dr. Thome's research here focused on microglial and neuroinflammatory mechanisms attributed to alpha-synuclein in models of Parkinson's disease. After graduation, he accepted an Edwards Post-Doctoral Fellowship at the Houston Methodist Neurological Institute under Stanley H. Appel, M.D., Edwards Distinguished Endowed Chair for ALS and Stanley H. Appel Department of Neurology Chair. Dr. Thome is currently primary faculty in the Houston Methodist Neurological Institute, Stanley H. Appel Department of Neurology, and Assistant Research Member for the Houston Methodist Research Institute.
Dr. Thome's research focuses on peripheral immune cells during the course of Alzheimer's disease (AD). Current trends in research focus primarily on microglia during the course of AD, justifiably, since they are the resident immune cell of the brain, are inflamed in late AD, and the genetics point to their dysfunction during disease. Expanding the examination of immune changes to the periphery is important on multiple fronts: 1) Permeability of the blood-brain barrier during AD provides a mechanism for peripheral immune cell infiltration. 2) Redundant disease-implicated genes and markers are also found in peripheral immune cells. 3) The increased understanding and analysis of neuro-immune crosstalk during health and disease provide cogent mechanisms for interactions between the brain and periphery.
Current research focuses:
1. Peripheral immune cell changes during the course of AD (populations, functions, and phenotypes)
2. The effects of peripheral immune changes on neuroinflammation and AD susceptibility/progression.
3. Translational immunomodulation for halting the progression of the disease.