Aimee Kao, MD, PhD

Professor in Residence
Department of Neurology
[email protected]
[email protected]
Research Overview: 

Despite intensive research efforts, many of the basic mechanisms underlying neurodegenerative diseases remain unclear.  We are tackling this problem by focusing on how aging, stress, gene variants and mutations alter protein homeostasis and lysosome function to predispose to neurodegeneration. Our recent work includes studies on the normal and abnormal metabolism of tau, TDP-43, progranulin and alpha-synuclein with a focus on how they are degraded by the proteases in the lysosome. We also consider how the lysosome function is regulated, including via pH set point and protease maturation.

For a recent overview of some of our work, please watch the video at this link. 

Primary Thematic Area: 
Neurobiology
Secondary Thematic Area: 
Human Genetics
Research Summary: 
Pathophysiology of Neurodegenerative Diseases: Aging, Stress, Lysosomes and Protein Homeostasis.
Mentorship Development: 

4/26/19    Sharpening your Mentoring Skills (SyMS) with Sharon Milgram (Mission Bay)    
11/23/20    Building Community in the UCSF MSTP 
9/11/20    Mentoring Across Differences
2/18/21    Three Truths and Three Tries: Facing and Overcoming Critical Social Justice Challenges at the Micro, Mezzo, and Macro Levels    

Websites

Publications: 

The relationship between caloric intake and clinical outcomes in critically ill patients: A retrospective study.

Clinical nutrition ESPEN

Lin YR, Chen PC, Li WT, Huang MH, Huang SF, Wang CJ, Chien YW, Kao AW, Shan YS

mTOR activation induces endolysosomal remodeling and nonclassical secretion of IL-32 via exosomes in inflammatory reactive astrocytes.

Journal of neuroinflammation

Leng K, Rooney B, McCarthy F, Xia W, Rose IVL, Bax S, Chin M, Fathi S, Herrington KA, Leonetti M, Kao A, Fancy SPJ, Elias JE, Kampmann M

Second international symposium on the chaperone code, 2023.

Cell stress & chaperones

Buchner J, Alasady MJ, Backe SJ, Blagg BSJ, Carpenter RL, Colombo G, Gelis I, Gewirth DT, Gierasch LM, Houry WA, Johnson JL, Kang BH, Kao AW, LaPointe P, Mattoo S, McClellan AJ, Neckers LM, Prodromou C, Rasola A, Sager RA, Theodoraki MA, Truman AW, Truttman MC, Zachara NE, Bourboulia D, Mollapour M, Woodford MR

Correction: Mutations in α-synuclein, TDP-43 and tau prolong protein half-life through diminished degradation by lysosomal proteases.

Molecular neurodegeneration

Sampognaro PJ, Arya S, Knudsen GM, Gunderson EL, Sandoval-Perez A, Hodul M, Bowles K, Craik CS, Jacobson MP, Kao AW