Cathleen (Cat) Lutz, Ph.D., M.B.A.

Senior Director, Mouse Repository & In Vivo Pharmacology Genetic Resource Science / Senior research scientist

The primary research goals of the Lutz lab involve developing preclinical mouse models of neurodegeneration to test therapeutics and inform clinical trials.

Contact me at: 207-288-6341

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About Cathleen (Cat) Lutz, Ph.D., M.B.A.

Dr. Lutz is Director of the Mouse Repository and the Rare and Orphan Disease Center at The Jackson Laboratory. She has fiscal and managerial oversight of a growing collection of more than 8,500 unique strains, including over 1,700 live colonies for distribution to the scientific community. As part of the Mouse Repository program, Dr. Lutz is the Principal investigator on a number of NIH sponsored resource grants, including the Mutant Mouse Regional and Research Center at JAX, The SMSR grant to support recombinant inbred and Chromosome substitution panels, as well as the NICHD Cytogenetic Resource to support Down Syndrome related strains and research. Dr. Lutz also serves as the Director of In Vivo Pharmacology and Efficacy Testing Program in Bar Harbor, which interfaces with biotechnology and pharmaceutical companies to pursue novel therapeutics across a variety of therapeutic areas.

A neuroscientist by training, Dr. Lutz conducts research in neurodegenerative diseases, including Spinal Muscular Atrophy (SMA), Friedreich’s ataxia, Amyotrophic Lateral Sclerosis (ALS) and Frontotemperal Lobe Dementia (FTD. Her lab works closely with multiple disease foundations and researchers in the development, characterization and validation of mouse models that support their research and drug discovery goals. These organizations include The ALS Association, The Friedreich’s Ataxia Research Alliance, the Spinal Muscular Atrophy (SMA) Foundation, Cure SMA, and the Grace Science Foundation.

Education and experience

Education

1997
Ph.D., biochemistry
University of Maine, Orono, ME

1990
B.S., biochemistry
The University of Pittsburgh, Pittsburgh, PA

Experience

2012-
Director, Rare and Orphan Disease Center, The Jackson Laboratory, Bar Harbor, ME

2011-
Director, Repository, and Research Scientist, Genetic Resource Science, The Jackson Laboratory, Bar Harbor, ME

2008-2011
Associate Director and Research Scientist, Genetic Resource Science, The Jackson Laboratory, Bar Harbor, ME

2004-2008
Mouse Repository Operations Manager and Associate Research Scientist, The Jackson Laboratory, Bar Harbor, ME

1998-2004
Senior Scientific Curator, Mouse Genome Informatics, The Jackson Laboratory, Bar Harbor, ME

1996-1998
Postdoctoral Associate, Laboratory of Dr. David Hosford, Duke University, Durham North Carolina

1993-1996
Predoctoral Associate, Laboratory of Dr. Wayne Frankel, The Jackson Laboratory, Bar Harbor, ME

1991-1993
Senior Research Assistant, Laboratory of Dr. Wayne Frankel, The Jackson Laboratory, Bar Harbor, ME

1990-1991
Research Assistant, Laboratory of Dr. Benjamin Taylor, The Jackson Laboratory, Bar Harbor, ME

1987-1990
Research Technician, Laboratory of Dr. Mary Edmonds, The University of Pittsburgh, Pittsburgh, PA

Selected Publications

Highlighted Abstract

Spinal muscular atrophy (SMA) is a common neuromuscular disorder in humans. In fact, it is the most frequently inherited cause of infant mortality, being the result of mutations in the survival of motor neuron 1 (SMN1) gene that reduce levels of SMN protein. Restoring levels of SMN protein in individuals with SMA is perceived to be a viable therapeutic option, but the efficacy of such a strategy once symptoms are apparent has not been determined. We have generated mice harboring an inducible Smn rescue allele and used them in a model of SMA to investigate the effects of turning on SMN expression at different time points during the course of the disease. Restoring SMN protein even after disease onset was sufficient to reverse neuromuscular pathology and effect robust rescue of the SMA phenotype. Importantly, our findings also indicated that there was a therapeutic window of opportunity from P4 through P8 defined by the extent of neuromuscular synapse pathology and the ability of motor neurons to respond to SMN induction, following which restoration of the protein to the organism failed to produce therapeutic benefit. Nevertheless, our results suggest that even in severe SMA, timely reinstatement of the SMN protein may halt the progression of the disease and serve as an effective postsymptomatic treatment.

View full list of publications

Featured ArticleOctober 22, 2018
A new world of opportunity in rare diseases
JAX neuroscientist Cat Lutz, Ph.D., gave a TED-style talk about strides in rare disease research as part of the Laboratory’s JAXtaposition speaker series. Photo by Brian Fitzgerald.
Search MagazineFebruary 28, 2017
Our mouse model paved the way for a new SMA drug
A mouse model of spinal muscular atrophy developed at The Jackson Laboratory lay the foundation for the successful clinical trials of a new SMA drug, Spinraza.
Search MagazineJanuary 06, 2016
The top 10 JAX stories of 2015
The Jackson Laboratory generated many exciting and newsworthy research discoveries and advances in 2015 that accelerated progress in the search for new cures to diseases that are rooted in our DNA. Here are our top 10 stories of 2015.
Press ReleaseOctober 14, 2015
Jackson Laboratory researchers report some restored function in animal models of spinal muscular atrophy
In work involving several new generations of mouse model development, Jackson Laboratory (JAX) researchers have tested a therapeutic intervention for spinal muscular atrophy (SMA) that restores some function lost due to a mutation in one gene (SMN1) and amplifies the levels of protective genes (SMN2). Moreover, unlike current interventions, the therapy appears to work after symptoms of SMA have already appeared, and may not need to be administered directly into the central nervous system.

Press ReleaseOctober 09, 2018
Advancing therapeutic gene editing
NIH awards $3.5M to JAX under multi-institution Somatic Cell Genome Editing program.
Search MagazineJanuary 17, 2017
Rethinking the mouse model in drug development
Australian researcher Sarah Stephenson wanted to fast-track her research of Parkinson's disease, so she shuffled the genetic deck using a new experimental platform at The Jackson Laboratory.
Research HighlightDecember 07, 2015
New mouse model displays typical pathologic features of ALS/FTD
Most cases of amyotrophic lateral sclerosis (ALS) are sporadic, meaning that there is no family history of the disease.
eNewsDecember 12, 2014
Collaborative efforts expand ALS research tools
Scientists are rapidly engineering mice that model these genetic lesions which will be critical for understanding pathogenesis of these diseases.