Aimee Kao, MD, PhD

Associate Professor

The molecular basis neurodegenerative diseases

Neurodegenerative diseases are fundamentally the result of aberrant proteostasis within neurons. My lab is interested in understanding the basic cell and molecular changes leading to this aberrant proteostasis in Alzheimer Disease, frontotemporal lobar degeneration and other neurodegenerative conditions. In particular, we are focused on the consequences of impaired autophagy and lysosomal function. The lysosome is not only the cell’s garbage can—rather, it is a central regulator of homeostasis, responsible for protein and lipid recycling, amino acid storage, appropriate stress response and regulated cell growth. We have shown that mutations responsible for neurodegenerative diseases can directly alter lysosome function with pleotropic downstream consequences. Our current work utilizes C. elegans, induced pluripotent stem cells (iPSC) and other cellular models to decipher how alterations in lysosome function, autophagy, cell and organelle pH and stress response programs can lead to neuronal dysfunction and death.

Current Projects

  • Granulins as inhibitors of lysosomal cathepsin activity
  • Regulated cleavage of progranulin into granulins
  • Modulation of ER stress in the pathogenesis of tauopathies
  • The mTOR pathway in autophagy regulation
  • Dysregulation of pH dynamics in Alzheimer Disease pathogenesis

Lab Members

Victoria Butler, PhD
Postdoctoral Fellow
[email protected]

Swetha Mohan
Postdoctoral Fellow
[email protected]

Carolina Alquezar Burillo, PhD
Postdoctoral Fellow
[email protected]

Andrea Argouarch
Assistant Specialist
[email protected]

Loan Doan
Lab Assistant
[email protected]