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

Albert (Gus) Davis, MD, PhD

Assistant Professor of Neurology
Adult, Movement Disorders

  Davis lab

Top areas of adult care: Parkinson’s disease, Lewy body dementia, tremor

Recent publications

  • Neocortical Lewy Body Pathology Parallels Parkinson's Dementia, but Not AlwaysMartin, W. R. W., Younce, J., Campbell, M., Racette, B., Norris, S., Ushe, M., Criswell, S., Davis, G., Alfradique-Dunham, I., Maiti, B., Cairns, N. J., Perrin, R. J., Kotzbauer, P. T. & Perlmutter, J. S., Jan 2023, In: Annals of neurology. 93, 1, p. 184-195 12 p.Research output: Contribution to journal › Article › peer-review
  • Solving neurodegeneration: common mechanisms and strategies for new treatmentsWareham, L. K., Liddelow, S. A., Temple, S., Benowitz, L. I., Di Polo, A., Wellington, C., Goldberg, J. L., He, Z., Duan, X., Bu, G., Davis, A. A., Shekhar, K., Torre, A. L., Chan, D. C., Canto-Soler, M. V., Flanagan, J. G., Subramanian, P., Rossi, S., Brunner, T., Bovenkamp, D. E., & 1 othersCalkins, D. J., Dec 2022, In: Molecular neurodegeneration. 17, 1, 23.Research output: Contribution to journal › Review article › peer-review
  • VCP suppresses proteopathic seeding in neuronsZhu, J., Pittman, S., Dhavale, D., French, R., Patterson, J. N., Kaleelurrrahuman, M. S., Sun, Y., Vaquer-Alicea, J., Maggiore, G., Clemen, C. S., Buscher, W. J., Bieschke, J., Kotzbauer, P., Ayala, Y., Diamond, M. I., Davis, A. A. & Weihl, C., Dec 2022, In: Molecular neurodegeneration. 17, 1, 30.Research output: Contribution to journal › Article › peer-review
  • CSF tau microtubule-binding region identifies pathological changes in primary tauopathiesHorie, K., Barthélemy, N. R., Spina, S., VandeVrede, L., He, Y., Paterson, R. W., Wright, B. A., Day, G. S., Davis, A. A., Karch, C. M., Seeley, W. W., Perrin, R. J., Koppisetti, R. K., Shaikh, F., Lago, A. L., Heuer, H. W., Ghoshal, N., Gabelle, A., Miller, B. L., Boxer, A. L., & 2 othersBateman, R. J. & Sato, C., Dec 2022, In: Nature medicine. 28, 12, p. 2547-2554 8 p.Research output: Contribution to journal › Article › peer-review
  • Pleiotropic effect of LRRK2 on Parkinson-associated proteins and processing of pathological alpha-synuclein in myeloid cellsNykanen, L. N-P., Yang, C., Harari, O., Davis, G., Cruchaga, C. & Benitez Viloria, B. A., Dec 2022, In: Alzheimer's and Dementia. 18, S4, e063954.Research output: Contribution to journal › Comment/debate