Positions
- Professor
-
Department of Neuroscience
Departments of Molecular and Cellular Biology, Neurology, and Neurosurgery
Baylor College of Medicine
Houston, TX
- Associate Director
-
Graduate Program in Neuroscience
Baylor College of Medicine
- Faculty Member
-
Graduate Programs in Neuroscience and Development, Disease Models, and Therapeutics (DDMT)
Baylor College of Medicine
- Vivan L. Smith Endowed Chair in Neuroscience
-
Baylor College Of Medicine
Addresses
- Department of Neuroscience (Lab)
-
Baylor College of Medicine
Houston, TX, 77030
United States
Education
- BA from Amherst College
- 06/1991 - Amherst, Massachusetts, United States
- Biology
- PhD from California Institute Of Technology
- 06/1999 - Pasadena, California, United States
- Molecular and Cellular Neuroscience
- Advanced Training from Johns Hopkins University School Of Medicine
- 01/2003 - Baltimore, MD, United States
Professional Statement
Our research focuses on the pathogenesis of Alzheimer’s disease. Broadly speaking, we want to understand factors that influence disease risk and dictate the stereotyped loss of neural circuits needed for memory. More specifically, we want to understand how aging increases the likelihood of dementia, how genetics may influence this risk, and how specific brain areas are selectively affected.
Our laboratory uses transgenic mice as a model system that can be engineered to reproduce focused aspects of the disease. These models allow us to test cellular and molecular hypotheses about causes and consequences of disease pathology, and to define how interactions between genes, environment, and aging determine resilience or risk.
We are currently pursuing three avenues of study. One project explores the genetic basis of cognitive reserve by engineering mice to express a gene variant associated with preserved cognition in patients with Alzheimer's neuropathology. Complementary studies examine how brain aging contributes to Alzheimer's risk using mice designed to stop time through exogenous control of amyloid onset. Finally, we are investigating the basis for progressive neuronal vulnerability in Alzheimer's using mice created to test whether circuit function contributes to disease susceptibility. Our hope is that mice and men share sufficient similarities in genetic architecture, basic physiology, and neuronal circuitry to gain insight from one useful in understanding the other.
Key questions:
1. How do genetics influence whether individuals with amyloid pathology will progress to dementia or remain cognitively healthy?
2. How does aging contribute to AD? Why does this disease primarily strike late in life?
3. What makes neurons of the entorhinal cortex particularly vulnerable in AD? Might their normal role in episodic memory contribute to their frailty in disease?
Our laboratory uses transgenic mice as a model system that can be engineered to reproduce focused aspects of the disease. These models allow us to test cellular and molecular hypotheses about causes and consequences of disease pathology, and to define how interactions between genes, environment, and aging determine resilience or risk.
We are currently pursuing three avenues of study. One project explores the genetic basis of cognitive reserve by engineering mice to express a gene variant associated with preserved cognition in patients with Alzheimer's neuropathology. Complementary studies examine how brain aging contributes to Alzheimer's risk using mice designed to stop time through exogenous control of amyloid onset. Finally, we are investigating the basis for progressive neuronal vulnerability in Alzheimer's using mice created to test whether circuit function contributes to disease susceptibility. Our hope is that mice and men share sufficient similarities in genetic architecture, basic physiology, and neuronal circuitry to gain insight from one useful in understanding the other.
Key questions:
1. How do genetics influence whether individuals with amyloid pathology will progress to dementia or remain cognitively healthy?
2. How does aging contribute to AD? Why does this disease primarily strike late in life?
3. What makes neurons of the entorhinal cortex particularly vulnerable in AD? Might their normal role in episodic memory contribute to their frailty in disease?
Selected Publications
-
Nguyen, Q. Wood, C.A., Kim, P.J, and Jankowsky, J.L.. " The TMEM106B T186S coding variant increases neurite arborization and synaptic density in primary hippocampal neurons " Front. Neurosci.. 2023 ;
Pubmed PMID: 37901434. -
50. Zhang, T., Pang, W., Feng, T., Guo, J., Wu, K., Nunez Santos, M., Arthanarisami, A., Nana, A.L., Nguyen, Q., Kim, P.J., Jankowsky, J.L., Seeley, W.L., Hu, F.. " TMEM106B regulates microglial proliferation and survival in response to demyelination " Sci Adv. 2023 ;
Pubmed PMID: 37146150. -
48. Koller, E.J., Comstock, M., Bean, J.C., Escobedo, G., Park, K.-W., Jankowsky, J.L.. " Temporal and spatially-controlled APP transgene expression using Cre-dependent alleles " 2022 ;
Pubmed PMID: 35394029. -
49. Zhao, R.*, Grunke, S.D.*, Wood, C.A.*, Perez, G.A., Comstock, M., Li, M.-H., Singh, A.K., Park, K.-W., Jankowsky, J.L.. " Activity disruption causes degeneration of entorhinal neurons in a mouse model of Alzheimer’s circuit dysfunction " eLife. 2022 ;
Pubmed PMID: 36468693.
Log In to edit your profile