Brian Wainger, MD, PhD, of the Healey Center for ALS at Massachusetts General Hospital presented initial clinical trial results at Motor Neurone Disease Association meeting.
Departments, Centers, & Programs:
Center for Pain Medicine
15 Parkman Street
Boston, MA 02114-3117
- MD, PhD, Columbia University College of Physicians and Surgeons
- Residency, Brigham and Women's Hospital
- Fellowship, Massachusetts General Hospital
American Board Certifications
- Neurology, American Board of Psychiatry and Neurology
- Pain Medicine, American Board of Psychiatry and Neurology
Accepted Insurance Plans
Brian Wainger's lab fuses electrophysiology and stem cell biology to explore how abnormal neuronal physiology contributes to diseases of the motor and sensory nervous systems. Working with motor neurons derived from ALS patients and healthy controls, Dr. Wainger performed fundamental electrophysiological characterization and identified motor neuron hyperexcitability in ALS patient-derived motor neurons (Wainger et al., 2014). Mechanistic analysis of the motor neurons led to the identification of a novel therapeutic candidate, which will be investigated in a clinical trial.
On the sensory neuron front, Dr. Wainger developed a lineage reprogramming technique for derivation of pain sensing (nociceptor) neurons from human fibroblasts (Wainger et al., 2014). This technology has already revealed novel insights through disease modeling of familial painful neuropathy and promises to be valuable in the development of drug screens using human neurons.
- Wainger BJ, Buttermore ED, Oliveira JT, Mellin C, Lee S, Afshar Saber W, Wang A, Ichida JK, Chiu IM, Barrett L, Huebner EA, Bilgin C, Tsujimoto N, Brenneis C, Rubin LL, Eggan K, Woolf CJ. Modeling pain in vitro using noceptors reprogrammed from fibroblasts. Nature Neuroscience, 2014, in press.
- Wainger BJ, Kiskinis EK, Mellin C, Wiskow O, Han S, Sandoe J, Perez NP, Williams AL, Lee S, Boulting G, Berry JD, Brown RH, Cudkowicz ME, Bean BP, Eggan K, Woolf CJ. Intrinsic membrane hyperexcitability of ALS patient-derived motor neurons. Cell Reports 2014;7:1-11