McLaughlin Institute

New Research Projects at MRI

MRI researchers Mike Kavanaugh, Teresa Gunn, and Deb Cabin began work this summer on a new genetically engineered mouse model of a common inherited neurotransmitter transporter gene mutation that causes cognitive and developmental delay in children. The team aims to determine the genetic and physiological mechanisms underlying the disorder, and they will test a novel therapeutic approach to treat the disorder using a drug developed at the University of Montana School of Pharmacy. Preliminary studies with the new drug have also suggested that it represents a new potential approach to treat schizophrenia.

Dr. Teresa Gunn received a grant from the National Institutes of Health to collaborate with GeneSearch, Inc. of Bozeman, Montana, to develop new technologies that will streamline the creation of mouse models of human disease. The work is opening up new possibilities to more rapidly advance understanding of the genetic basis of human disease.

MRI researchers and Harvard/MIT collaborators Sonia Vallabh and Eric Minikel launched a preclinical trial this fall at MRI to test a new gene-silencing approach to treat prion disease. In the ongoing trial, the team is using a new DNA-based drug from Ionis Pharmaceuticals to treat the disease in mice, with the ultimate aim to translate the treatment to human disease. Sonia and Eric spoke at MRI two years ago about their journey into prion research with guidance from MRI. Sonia carries the gene for Fatal Familial Insomnia, a prion disease that killed her mother at age 52, and they are racing against the clock to find a way to save Sonia and others like her from this dreadful disease.

McLaughlin Research Institute and collaborators at Columbia University received three grants this year from the National Institutes of Health to support research at MRI with mouse models of Alzheimer’s disease. The mice are genetically engineered to recapitulate human mutations linked to Alzheimer’s disease. Studies with these mice will provide critical information to understand the pathological mechanism of changes in genes such as the ApoE4 allele, which are associated with increased prevalence of the disease.


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