Personal profile
Research interests
Tau dysfunction is implicated in many neurodegenerative diseases, including Alzheimer’s disease, frontotemporal dementia, progressive supranuclear palsy, corticobasal degeneration, and Pick’s disease. Most of these diseases are characterized by tau protein aggregation and are termed tauopathies. In these diseases, tau is affected at the molecular (splicing), protein (hyperphosphorylation, cleavage, aggregation), and cellular (secretion) levels. Thus, defining the molecular mechanisms underlying tauopathies require unraveling the complexities of the MAPT gene that encodes the tau protein, tau protein dysfunction within the cell, and the cell-cell interactions that produce pathology in the human brain. We use traditional immortalize and human induced pluripotent stem cell-derived neuron and astrocytes to define the molecular and cellular mechanisms underlying tauopathies.
Mentoring
Our goal is to perform cutting-edge research to understand and cure neurodegenerative disease, while advocating for equity and representation within and beyond the lab. As a lab, we understand and appreciate the desire to create a workplace that is not only diverse, but inclusive. We actively adapt our laboratory environment to ensure that individuals of different backgrounds, beliefs, and experiences are provided an atmosphere that fosters creativity and scientific discovery. We stand firmly against all forms of racism, oppression, and discrimination – both within our lab and our community. We seek to recruit individuals to join our laboratory community regardless of race, religion, ethnicity, sexual orientation, gender identity or expression, socioeconomic status, disability status, or immigration and citizenship status.
Our laboratory has experienced tremendous success because of our dedication to diversity and inclusion. As scientists, we must be able to utilize the mentorship and comradery of our lab mates to ensure our success. We strongly encourage collaborative efforts, both within and outside the lab, to address important medical and socially relevant questions related to neurodegeneration. These collaborative efforts not only help us accomplish our project-specific goals but also construct a solid framework of growth and support for all lab members. When providing mentorship to trainees, the Karch Lab recognizes how important an appropriate work-life balance, flexibility, and teamwork can be. We firmly believe that providing these attributes to our lab members will result in a continued passion and enthusiasm for scientific inquiry.
Available to Mentor:
- Undergraduate Students
- Post-Baccalaureate Students
- PhD Students
- Health Professions (Medical, OT, PT, Dental, Audiology, etc.) Students
- Postdocs
- Residents and Fellows
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Collaborations and top research areas from the last five years
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A pathogenic Tau mutation drives autophagy-lysosome dysfunction that limits Tau degradation in a model of frontotemporal dementia
Mirfakhar, F. S., Marsh, J. A., Sato, C., Schache, K. J., Minaya, M. A., Dolle, R. E., Pak, S. C., Silverman, G. A., Perlmutter, D. H., Macauley, S. L. & Karch, C. M., Dec 2026, In: Nature communications. 17, 1, 2699.Research output: Contribution to journal › Article › peer-review
Open Access2 Link opens in a new tab Scopus citations -
Cortical asymmetry in autosomal dominant Alzheimer’s disease progression
Pérez-Millan, A., Falgàs, N., Bosch, B., Borrego-Écija, S., Antonell, A., Fernández-Villullas, G., Esteller-Gauxax, D., Tort-Merino, A., Bargalló, N., Balasa, M., Lladó, A., Aguillon, D., Chrem, P., Day, G. S., Devenney, E., Huey, E. D., Ikeuchi, T., Jucker, M., Kasuga, K. & Vöglein, J. & 119 others, , 2026, In: Brain Communications. 8, 1, fcaf488.Research output: Contribution to journal › Article › peer-review
Open Access -
Inducible deletion of DGAT1 and 2 from microglia exacerbates neurodegeneration and endolysosomal lipid accumulation in male PS19 mice
Tabor, G. T., Litvinchuk, A., Chen, Y., Allison, A., Sun, E. W., van Lengerich, B., Davis, S. S., West, E., Schlachetzki, J. C. M., Zeng, C., Hu, H., Lin, P. B., Sharma, P., Chen, X., Parhizkar, S., Song, S., Bao, X., Senthil, L., Iyer, A. K. & You, S. F. & 17 others, , Jan 27 2026, In: Cell Reports. 45, 1, 116841.Research output: Contribution to journal › Article › peer-review
Open Access -
Integrative genomic and functional analyses reveal NINL as a modulator of tau aggregation
Swift, S. K., Huang, G., Cochran, J. N., D'Oliveira Albanus, R., Minaya, M. A., Castruita, P. A., Zhang, R., Miller, K. J., Starr, E., Galasso, G., Marsh, J. A., Kao, A. W., Harari, O., Yokoyama, J. S. & Karch, C. M., Apr 2026, In: Alzheimer's and Dementia. 22, 4, e71352.Research output: Contribution to journal › Article › peer-review
Open Access -
Longitudinal subcortical volume changes and their correlations with multiple PET and fluid biomarkers in dominantly inherited Alzheimer’s disease
Choo, I. H., Park, H., Gordon, B. A., Bateman, R. J., Bateman, R., Daniels, A. J., Courtney, L., Ziegemeier, A., Skrbec, K., Hellm, C., Martin, M., Ziegemeier, E., Bartzel, J., McDade, E., Libre-Guerra, J. J., Supnet-Bell, C., Xiong, C., Xu, X., Lu, R. & Wang, G. & 106 others, , Apr 2026, In: Journal of Prevention of Alzheimer's Disease. 13, 4, 100513.Research output: Contribution to journal › Article › peer-review
Open Access