PiN Faculty Member - Matthew LaVoie, PhD

Matthew LaVoie, PhD

Associate Professor of Neurology

Brigham and Women's Hospital
Ann Romney Center for Neurologic Diseases
60 Fenwood Road, BTM 10016M
Boston, MA 02115
Tel: 617-525-5185
Fax: 617-525-5252
Visit my lab page here.

The LaVoie lab is interested in the earliest molecular events that ultimately culminate in the premature demise of neurons in adult-onset neurodegenerative disease such as Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, and Huntington's disease. To uncover these pathogenic pathways at mechanistic detail we use a variety of models including cell lines, iPSC-derived neurons and glia, and knockin mouse models to examine genetic factors that unequivocally cause disease. We apply rigorous biochemical, molecular, and imaging-based approaches to these models, and have incorporated CRISPR/Cas9 gene editing to generate additional synthetic models of disease.

Autosomal dominant mutations in the gene encoding for LRRK2 represent the most common genetic cause of Parkinson’s disease (PD). We are interested in uncovering how missense mutations in LRRK2 affect the processing of aggregate-prone proteins by neurons and glia, and how LRRK2-PD might inform the pathways involved in sporadic PD, and other neurologic diseases such as Frontotemporal Dementia (FTD).

The lab is also interested in how mitochondrial dysfunction may contribute to neurologic disease, and how novel approaches to improve oxidative phosphorylation in neurons may be protective. This work involves a focus on proteins including parkin, PINK1, and mitochondrial chaperones also linked to neurodegeneration. Recent efforts are now leveraging new advances in mitochondrial biology towards therapeutic intervention in models of Huntington’s disease and amyotrophic lateral sclerosis, as well as PD.

Last Update: 9/16/2020


For a complete listing of publications click here.



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