Catherine Cahill, Ph.D.


Assistant Investigator
Psychiatry, Mass General Research Institute
Assistant Professor of Psychiatry
Harvard Medical School
PhD University College Dublin 1990
5' untranslated regions; alpha-synuclein genes; amyloid beta-protein precursor; amyloid precursor protein; cytokine; cytokine gene regulation; ferritins; growth factor; growth hormone; interleukin-1; intestinal inflammation; iron; protein biosynthesis; small molecule translation blockers

Dr. Cahill received her PhD from University College Dublin, Ireland and did her postdoctoral research in the Department of Immunology at the Babraham Research Institute, Cambridge, UK, and at Dana-Farber Cancer Institute and Harvard Medical School.

Her major research interests include:

  1. Gut-brain axis and systemic inflammation
  2. Development of IRE directed small molecules  to treat neurodegeneration and neurodevelopmental disorders
  3. White matter injury and neurodegeneration

The biochemical signaling pathways between the gastrointestinal tract and the central nervous system, referred to as the “gut-brain axis” is a bi-directional communication system which can be impaired in many neurodegenerative diseases including Alzheimer’s disease (AD), Parkinson’s disease (PD) and Down syndrome (DS). Systemic inflammation due to infection can play a major role. Dr. Cahill has discovered novel biochemical pathways involving the inflammation associated transcription factors, activator protein 1 (AP-1) and nuclear factor kappa B (NFkB) in the human intestine leading to increases in pro-inflammatory cytokines. These studies  have revealed therapeutic targets which may ultimately lead to therapies to accelerate delayed intestinal development in the premature infant and which are also relevant to inflammation and colon cancer.

Under her direction, the Neurochemistry Lab’s research portfolio has expanded to include the study of neurodevelopmental disorders including Down syndrome and her most recent research aims to understand the impact of early life stressors and environmental exposures, including lead, on the developing brain where neurodegenerative mechanisms may be at work earlier in life. Inflammation prior to birth, triggered by maternal infection, toxins or bad nutrition, including iron deficiency, may be an underlying mechanism. In collaboration with Dr. Rogers and Stanford University scientist Ahmad Salehi, PhD, Dr. Cahill proposes to test the potential of novel small molecule JTR-009 to treat Alzheimer’s disease associated Down syndrome (AD-DS). Down syndrome is associated with several abnormalities, including intellectual disability and early onset AD. Triplication of chromosome 21, containing the AD-associated amyloid precursor protein (APP) gene in DS means increased amyloid burden for these patients. The aim is to modulate APP in early fetal development in a mouse model of DS and moving from “bench to bedside,” to identify periods when the administration of therapeutic molecules such as JTR-009 would have a protective effect.