- Graduate School - Northwestern University Feinberg School of Medicine (2005-2012), Neuroscience
- Medical School - Northwestern University Feinberg School of Medicine (2010-2014)
- Internship - UT Southwestern Medical Center (2014-2015), Internal Medicine
- Other Post Graduate Training - Northwestern University Feinberg School of Medicine (2005-2012)
- Residency - UT Southwestern Medical Center (2015-2018), Neurology
- Fellowship - UT Southwestern Medical Center (2018-2020), Behavioral Neurology
Brian Hitt, M.D., Ph.D.
Brian Hitt, M.D., Ph.D., is an Assistant Professor in the Behavioral Neurology section of UT Southwestern Medical Center’s Department of Neurology. He specializes in neurodegenerative diseases and conducts basic science and translational research aimed at better understanding the molecular mechanisms of neurodegeneration and developing new diagnostic techniques.
Dr. Hitt earned his B.S. in Neurobiology and Behavior from the University of California, Irvine and his M.D. and Ph.D from Northwestern University Feinberg School of Medicine. There his research focused on the molecular events leading to the formation of the beta amyloid peptide that is central to Alzheimer’s disease pathology.
Dr. Hitt completed his residency in Neurology and a fellowship in Behavioral Neurology at UT Southwestern Medical Center prior to joining the faculty. He is certified by the American Board of Psychiatry and Neurology and is a member of the American Academy of Neurology and the International Society to Advance Alzheimer’s Research and Treatment.
Dr. Hitt’s laboratory-based research at UT Southwestern’s Center for Alzheimer’s and Neurodegenerative Disease focuses on the role of the tau protein in the progression of diseases like Alzheimer’s disease, frontotemporal dementia, and progressive supranuclear palsy. It aims to find new ways to detect the structural changes in tau protein associated with different diseases, allowing for more specific diagnosis and characterization of pathology, and informing efforts to develop disease-modifying therapies. As part of UT Southwestern’s Alzheimer’s Disease Center for clinical research, Dr. Hitt also works with research participants to improve the care of patients with Alzheimer’s disease and related disorders. His research is supported by the Alzheimer’s Association.
Clinically, Dr. Hitt is committed to providing the highest quality care for patients with neurodegenerative diseases and other disorders of cognition and behavior, and educating patients and their loved ones about these conditions.
- Society for Neuroscience (2008-2020)
- International Society to Advance Alzheimer's Research and Treatment (2008-2020)
- American Academy of Neurology (2014-2020)
- Alzheimer's Association Clinician Scientist Fellowship 2018
- UT Southwestern Integrated Program for the Advancement of Neuroscience Research Careers 2016-2020
- Northwestern University Cell and Molecular Basis of Disease Training Program 2008-2012
- Excellence in Research, University of California Irvine 2003
Presenilin regulates capacitative calcium entry dependently and independently of gamma-secretase activity.
Akbari Y, Hitt BD, Murphy MP, Dagher NN, Tseng BP, Green KN, Golde TE, LaFerla FM Biochemical and biophysical research communications 2004 Oct 322 4 1145-52
Enhanced caffeine-induced Ca2+ release in the 3xTg-AD mouse model of Alzheimer's disease.
Smith IF, Hitt B, Green KN, Oddo S, LaFerla FM, Journal of neurochemistry 2005 Sep 94 6 1711-8
Phosphorylation of the translation initiation factor eIF2alpha increases BACE1 levels and promotes amyloidogenesis.
O'Connor T, Sadleir KR, Maus E, Velliquette RA, Zhao J, Cole SL, Eimer WA, Hitt B, Bembinster LA, Lammich S, Lichtenthaler SF, Hébert SS, De Strooper B, Haass C, Bennett DA, Vassar R, Neuron 2008 Dec 60 6 988-1009
SERCA pump activity is physiologically regulated by presenilin and regulates amyloid beta production.
Green KN, Demuro A, Akbari Y, Hitt BD, Smith IF, Parker I, LaFerla FM The Journal of cell biology 2008 Jun 181 7 1107-16
BACE1-/- mice exhibit seizure activity that does not correlate with sodium channel level or axonal localization.
Hitt BD, Jaramillo TC, Chetkovich DM, Vassar R Molecular neurodegeneration 2010 Aug 5 31
ß-Site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1)-deficient mice exhibit a close homolog of L1 (CHL1) loss-of-function phenotype involving axon guidance defects.
Hitt B, Riordan SM, Kukreja L, Eimer WA, Rajapaksha TW, Vassar R, The Journal of biological chemistry 2012 Nov 287 46 38408-25
Beta-site amyloid precursor protein cleaving enzyme 1 levels become elevated in neurons around amyloid plaques: implications for Alzheimer's disease pathogenesis.
Zhao J, Fu Y, Yasvoina M, Shao P, Hitt B, O'Connor T, Logan S, Maus E, Citron M, Berry R, Binder L, Vassar R, The Journal of neuroscience : the official journal of the Society for Neuroscience 2007 Apr 27 14 3639-49
- Presenilin regulates capacitative calcium entry dependently and independently of gamma-secretase activity.
- Neurodegenerative Diseases
- Diseases of tau protein
- Biomarker development