Davis Lab
Albert (Gus) Davis, MD
Parkinson disease and dementia with Lewy bodies are neurodegenerative illnesses that result in progressive motor impairment, dementia, and psychosis. These disorders share the common feature of accumulation of insoluble aggregates of the protein alpha-synuclein (aSyn) into inclusions termed Lewy bodies. The molecular and cellular mechanisms that regulate aggregation of aSyn are not well understood, and there are currently no disease-modifying therapies for this class of disorders, termed synucleinopathies. Although aSyn is an abundant brain protein that plays a normal role in neuronal synaptic function, specific aggregated forms of aSyn are toxic and have been used to induce neuron dysfunction and injury in experimental models of synucleinopathy. We use a combination of in vitro, cell culture, and in vivo model systems to investigate the molecular and cellular mechanisms responsible for pathological aggregation of aSyn and neurodegeneration. The primary goal of our research is to increase our understanding of the basic pathophysiological mechanisms underlying protein aggregation and neurodegeneration in synucleinopathies in order to pave the way for improved diagnostic tests and disease-modifying treatments for these illnesses.
Principal investigator
Albert (Gus) Davis, MD, PhD
Assistant Professor of Neurology
Adult, Movement Disorders
Recent publications
- HTRA1 disaggregates α-synuclein amyloid fibrils and converts them into non-toxic and seeding incompetent speciesChen, S., Puri, A., Bell, B., Fritsche, J., Palacios, H. H., Balch, M., Sprunger, M. L., Howard, M. K., Ryan, J. J., Haines, J. N., Patti, G. J., Davis, G. & Jackrel, M. E., Dec 2024, In: Nature communications. 15, 1, 2436.Research output: Contribution to journal › Article › peer-review
- Concerns with the new biological research criteria for synucleinopathyNAPS co-investigators, Boeve, B. F., Davis, A. A., Ju, Y. E., Kantarci, K., Singer, W., Videnovic, A., Avidan, A., Bliwise, D., Boeve, B., Campbell, M., Criswell, S., Davis, A. “., Duff, K., Ehgoetz-Martens, K., Elliott, J., Ferman, T., Fields, J., Forsberg, L. & Gagnon, J. F. & 19 others, Gan-Or, Z., Howell, M., Hu, M., Hu, X., Huddleston, D., Kotzbauer, P., Langley, J., Lim, M., Lowe, V., McLeland, J., Miglis, M., Mignot, E., Neilson, L., Pelletier, A., Postuma, R., Ross, O., Schenck, C., St Louis, E. & Xiong, C., Jul 2024, In: […]
- Brain high-throughput multi-omics data reveal molecular heterogeneity in Alzheimer’s diseaseEteleeb, A. M., Novotny, B. C., Tarraga, C. S., Sohn, C., Dhungel, E., Brase, L., Nallapu, A., Buss, J., Farias, F., Bergmann, K., Bradley, J., Norton, J., Gentsch, J., Wang, F., Davis, A. A., Morris, J. C., Karch, C. M., Perrin, R. J., Benitez, B. A. & Harari, O., Apr 2024, In: PLoS biology. 22, 4 April, e3002607.Research output: Contribution to journal › Article › peer-review
- APOE3ch alters microglial response and suppresses Aβ-induced tau seeding and spreadChen, Y., Song, S., Parhizkar, S., Lord, J., Zhu, Y., Strickland, M. R., Wang, C., Park, J., Tabor, G. T., Jiang, H., Li, K., Davis, A. A., Yuede, C. M., Colonna, M., Ulrich, J. D. & Holtzman, D. M., Jan 18 2024, In: Cell. 187, 2, p. 428-445.e20Research output: Contribution to journal › Article › peer-review
- Neuronal deletion of the circadian clock gene Bmal1 induces cell-autonomous dopaminergic neurodegenerationKanan, M. K., Sheehan, P. W., Haines, J. N., Gomez, P. G., Dhuler, A., Nadarajah, C. J., Wargel, Z. M., Freeberg, B. M., Nelvagal, H. R., Izumo, M., Takahashi, J. S., Cooper, J. D., Davis, A. A. & Musiek, E. S., Jan 2024, In: JCI Insight. 9, 2, e162771.Research output: Contribution to journal › Article › peer-review