Xueyi Li, MD, PhD, has ongoing studies relating to Huntington’s disease and autism spectrum disorders.

Research Investigator Profile

Dr. Li

Xueyi Li, MD, PhD

  • Assistant Professor of Neurology,
    Harvard Medical School
  • Assistant in Neuroscience,
    Massachusetts General Hospital

 

 

Research Description

TIRF image of HD cell

Dr. Li studies molecular mechanisms of endosomal recycling, a process utilized by mammalian cells to retrieve internalized cell surface proteins for reuse, and explores strategies to harness endosomal recycling for therapeutic intervention in neurological disorders. Dr. Li’s early work at MIND uncovered that the causative mutation of Huntington’s disease compromises the function of Rab11, a critical modulator of endosomal recycling, and showed that augmentation of Rab11 function protects Huntington’s disease neurons die from causes triggered intrinsically or by exposure to harmful stimuli. His studies implicate that enhancing the function of Rab11 has great potential for treating Huntington’s disease. Dr. Li also investigates whether and how endosomal recycling is involved in the pathogenesis of neurodevelopmental disorders, e.g., autism spectrum disorders. Ongoing studies directed by Dr. Li involve validation of Rab11 as a therapeutic target for developing Huntington’s disease therapy and creation of new animal models of autism spectrum disorders.

Dr. Li is also a member of Dr. Marian Difiglia's Cellular Neurobiology Laboratory.

Research interests

Endosome dynamics, protein trafficking, drug discovery, animal behaviors

Research techniques

Gene targeting, microscopic imaging, RNAi, cell culture, protein trafficking assays

Diseases studied

Huntington’s disease and autism spectrum disorders

Selected publications
  1. Li X, Difiglia M. The recycling endosome and its role in neurological disorders. Prog Neurobiol. 2011 Oct 20.
  2. Li X, Valencia A, Sapp E, Masso N, Alexander J, Reeves P, Kegel KB, Aronin N, Difiglia M. Aberrant Rab11-dependent trafficking of the neuronal glutamate transporter EAAC1 causes oxidative stress and cell death in Huntington's disease. J Neurosci. 2010; 30: 4552-61.
  3. Li X, Standley C, Sapp E, Valencia A, Qin ZH, Kegel KB, Yoder J, Comer-Tierney LA, Esteves M, Chase K, Alexander J, Masso N, Sobin L, Bellve K, Tuft R, Lifshitz L, Fogarty K, Aronin N, DiFiglia M. Mutant huntingtin impairs vesicle formation from recycling endosomes by interfering with Rab11 activity. Mol Cell Biol. 2009; 29: 6106-16.
  4. Li X, Sapp E, Chase K, Comer-Tierney LA, Masso N, Alexander J, Reeves P, Kegel KB, Valencia A, Esteves M, Aronin N, Difiglia M. Disruption of Rab11 activity in a knock-in mouse model of Huntington's disease. Neurobiol Dis. 2009; 36: 374-83.
  5. Li X, Kaloyanova D, van Eijk M, Eerland R, van der Goot G, Oorschot V, Klumperman J, Lottspeich F, Starkuviene V, Wieland FT & Helms JB. Involvement of a GPI-anchored protein in maintenance of the Golgi structure. Mol Biol Cell, 2007; 18:1261-1271.
NCBI PubMed link NCBI PubMed publications
E-mail address xli12@partners.org
Lab mailing address Attention: Xueyi Li, MD, PhD
MassGeneral Institute for Neurodegenerative Disease (MIND)
Mailcode: CNY 114, Room 2150
114 16th Street
Charlestown, MA  02129

 

Updated 02/9/2012