Amy Rumora, PhD

  • Assistant Professor of Neurological Sciences (in Neurology)
Profile Headshot


Academic Appointments

  • Assistant Professor of Neurological Sciences (in Neurology)


  • Female

Credentials & Experience

Education & Training

  • Undergraduate, Mount Holyoke College
  • PhD, University of Vermont
  • Fellowship: University of Michigan

Honors & Awards

  • 2023 Berrie Pre-translational Diabetes Research Award
  • 2022 P30 Columbia Diabetes Research Center Pilot and Feasibility Award (NIH/NIDDK)
  • 2019 K99/R00 Pathway to Independence Award, NIH/NIDDK
  • 2017 Ruth L. Kirschstein Postdoctoral Independent National Research Service Award (F32), NIH/NIDDK
  • 2016 NEURODIAB Young Investigator Oral Presentation Award
  • 2015 Postdoctoral Institutional training grant recipient (NIH/NIDDK T32), University of Michigan
  • 2009 Predoctoral Institutional training grant recipient (NIH/NHLBI T32), University of Vermont


Research in my laboratory aims to identify molecular mechanisms underlying the development of peripheral neuropathy (PN), a common and disabling condition for patients with prediabetes and type 2 diabetes. PN is characterized by pain and eventual loss of sensation in the limbs that results from peripheral nerve damage. Although the cause of PN in type 2 diabetes and prediabetes is not completely understood, dyslipidemia has emerged as a major risk factor suggesting that dietary fatty acids may contribute to PN pathogenesis. We recently discovered that dietary saturated fatty acids (SFAs) and monounsaturated fatty acids (MUFAs) differentially regulate nerve function in murine models of prediabetes. We found that MUFAs reverse the progression of PN and improve nerve function in prediabetic murine models.

A major focus of my laboratory is to understand the molecular basis for the differential regulation of nerve function by SFAs and MUFAs. We use a combination of animal models, live-cell confocal imaging techniques, and molecular analyses to 1) assess the efficacy of MUFAs for restoring nerve function in models of prediabetes and type 2 diabetes, 2) identify the molecular mechanisms by which MUFAs improve nerve function, 3) evaluate the impact of dietary fatty acids on mitochondrial trafficking and function in sensory neurons, and 4) determine whether dietary SFAs and MUFAs differentially alter lipid levels within the nerve. Our long-term goal is to identify new mechanisms underlying neuropathy progression to support the development of mechanism-based therapies for neuropathy.

Research Interests:

  • Peripheral neuropathy
  • Diabetes, Obesity and Prediabetes
  • Sensory neuroscience
  • Mitochondrial dysfunction
  • Fatty acids
  • Sphingolipids