Our research focuses on how synaptic plasticity is impaired in neurodegenerative disease, with an emphasis on Alzheimer's disease. We are interested both in studying mechanisms of synaptic dysfunction as well as in identifying targets for therapeutic intervention. Specific issues we are currently focused on are:
1) I am interested in what beta-amyloid is normally doing in the brains of people without Alzheimer's disease. Beta-amyloid is present at low levels in the brain throughout life, and may have an important role in normal brain physiology. Ironically, there is some evidence that beta-amyloid actually facilitates neuronal connectivity and memory in people when it is present at low (normal) concentrations, and becomes toxic to neurons at higher concentrations. By studying its normal function and how it is regulated, we hope to understand better how it may accumulate in the brains of Alzheimer's patients.
2) We are using computational techniques to analyze genome expression data from neurons of Alzheimer's patients to determine whether there are any transcription factors that are primarily responsible for driving synaptic dysfunction in Alzheimer's disease. Transcription factors identified through this effort will be further studied as possible targets for therapeutic intervention.
, Patel M, Arancio O. A Reliable Way to Detect Endogenous Murine β-Amyloid. PLOS ONE. Feb 8(2):e55647, 2013.
Butler T, Ichise M, Teich AF
, Gerard E, Osborne J, French J, Devinsky O, Kuzniecky R, Gilliam F, Pervez F, Provenzano F, Goldsmith S, Vallabhajosula S, Stern E, Silbersweig D. Imaging Inflammation in a Patient with Epilepsy Due to Focal Cortical Dysplasia. J Neuroimaging. 2013 Jan 23(1):129-131.Teich AF
and Arancio O. Is the Amyloid Hypothesis of Alzheimer’s disease
therapeutically relevant? Biochemical Journal. 2012 Sep 1; 446(2): 165-77.
Hashimoto G, Sakurai M, Teich AF
, Saeed F, Aziz F, Arancio O. 5-HT4 Receptor Stimulation Leads to Soluble AβPPα Production through MMP-9 Upregulation. J. Alzheimers Disease. 32(2):437-45, 2012.
Qin Z, Luo J, Vandevrede L, Tavassoli E, Fa' M, Teich AF
, Arancio O, Thatcher GR. Design and Synthesis of Neuroprotective Methylthiazoles and Modification as NO-Chimeras for Neurodegenerative Therapy. J Med Chem. 2012 Aug 9;55(15):6784-801.Teich AF
, Hedley-Whyte ET, Goldman JE. “Pontinization” of the Medulla: Two Clinical
Case Studies. Neuropathol Appl Neurobiol. 37(6), 689-693, 2011.Teich AF
and Qian N. V1 orientation plasticity is explained by broadly tuned
feedforward inputs and intracortical sharpening. Visual Neuroscience 27: 57-73,
Zhiping P. Pang, Ernestina Melicoff, Daniel Padgett, Yun Liu, Teich AF
, Burton F. Dickey, Weichun Lin, Roberto Adachi, and Thomas C. Südhof. Synaptotagmin-2 Is Essential for Survival and Contributes to Ca2+ Triggering of Neurotransmitter Release in Central and Neuromuscular Synapses. Journal of Neuroscience 26: 13493 – 13504, 2006.Teich AF
and Qian N. Comparison Among Some Models of V1 Orientation Selectivity. Journal of Neurophysiology 96: 404-419, 2006.Teich AF
and Qian N. Learning and adaptation in a recurrent model of V1 orientation selectivity. Journal of Neurophysiology 89: 2086-2100, 2003.
Honors and Awards
- New Investigator Research Grant (NIRG) from the Alzheimer’s Association2011
- Louis V. Gerstner, Jr. Scholar Award2011
– New Investigator Research Grant (NIRG) from the Alzheimer’s Association2005
– PhD awarded from Columbia University with Distinction1998
– BA awarded from Cornell University magna cum laude with distinction in all subjects
Committees , Council, and Professional Society Memberships
Diplomate of the American Board of Pathology; Board Certification in Anatomic Pathology and Neuropathology
Active Member of the American Association of Neuropathologists
Member of the Society for Neuroscience
Professional Member of the International Society to Advance Alzheimer’s Research and Treatment (ISTAART)