Our Research

Cytokine (IL-1ß) and chemokine (CX3CL1) signaling in Alzheimer’s disease and other tauopathies

Our research program investigates how microglia-mediated neuroinflammation drives tau pathology. We are also exploring how build-up of pathological tau, in turn, triggers microglial activation. Our research specifically focuses on interleukin-1 (IL-1) and fractalkine (CX3CL1) signaling and a variety of cell culture (cell lines, iPSC and organoid), animal (conditional knockouts and transgenic) and human samples to understand this causal link. See selected publications below.

SELECTED PUBLICATIONS:

1. Bhaskar K et al., (2010). Neuron 68:1-13. (Video Abstract). PMID: 20920788. PMCID: PMC2950825.
2. Maphis, N, et al and Bhaskar K (2015). Brain Jun;138(Pt 6):1738-55. doi: 10.1093/brain/awv081. PMID: 25833819. PMCID: PMC4542622.
3. Bemiller S, et al., and Bhaskar K (2018). J. Neuroinflammation Sep 25;15(1):278). PMID: 30253780; PMCID: PMC6154806.
4. Jiang, S, et al., and Bhaskar, K (2021). Cell Reports 2021 Sep 21;36(12):109720. doi: 10.1016/j.celrep.2021.109720. PMID: 34551296.

Vaccines for Alzheimer’s disease

The other promising research program is developing vaccines for Alzheimer’s disease. A variety of disease-related tau epitopes and inflammatory targets are being tested on a virus-like particle (VLP) platform to generate and test novel vaccine for tau pathology.

Anti-tau roles of autophagy and proteosomal pathways

In a series of publications, we showed anti-tau effects of autophagy, which is another active area of research.