Carmo Costa , PhD
Biography
The Costa laboratory investigates mechanisms of neurodegeneration and conducts studies towards the development of therapeutics for neurodegenerative diseases.
Education
Post-doctoral fellow - Translational approaches for neurodegenerative diseases, Department of Neurology, University of Michigan, 2008
Ph.D. in Life and Biomedical Sciences, School of Medicine/ Life and Health sciences Research Institute, University of Minho, 2003
Licenciatura in Biochemistry, Faculty of Sciences/ Institute of Biomedical Sciences Abel Salazar, University of Porto, 1994
Employment
Assistant Professor (tenure system), Michigan State University, East Lansing, 2025 - Present
Research Assistant Professor , University of Michigan, Ann Arbor, 2017 - 2025
Research Investigator , University of Michigan, Ann Arbor, 2013 - 2017
Research Assistant, University of Porto, Porto, 1999 - 2003
Publications
Blood DDIT4 and TRIM13 Transcript Levels Mark the Early Stages of Machado–Joseph Disease Annals of Neurology (2025)
Blood and cerebellar abundance of ATXN3 splice variants in spinocerebellar ataxia type 3/Machado-Joseph disease. Neurobiology of disease (2024)
Blood levels of neurofilament light are associated with disease progression in a mouse model of spinocerebellar ataxia type 3 Disease Models & Mechanisms (2023)
Editorial: The role of posttranslational modifications in polyglutamine diseases. Frontiers in molecular neuroscience (2023)
Tissue-Specific Vulnerability to Apoptosis in Machado-Joseph Disease Cells (2023)
Regional and age-dependent changes in ubiquitination in cellular and mouse models of spinocerebellar ataxia type 3. Frontiers in molecular neuroscience (2023)
Blood DDIT4 and TRIM13 transcript levels mark the early stages of Machado-Joseph disease Biorxiv (2023)
Blood neurofilament light chain levels are associated with disease progression in a transgenic SCA3 mouse model Biorxiv (2023)
Sleep Alterations in a Mouse Model of Spinocerebellar Ataxia Type 3 Cells (2022)
Altered retinal structure and function in Spinocerebellar ataxia type 3. Neurobiology of disease (2022)
Fundings
Investigating the efficacy of aripiprazole related compounds as a therapeutic option for SCA3
Development of allele-specific gene therapeutic targeting the pathogenic RNA associated with Spinocerebellar ataxia type 3
Definition of the polyglutamine protein ataxin-3 interactome in the human retina.
#1 Development of therapeutics for polyglutamine diseases/ #2 Elucidation of gain-of-function and loss-of-function mechanisms of polyglutamine diseases in the brain
NIK as a therapeutic target for Spinocerebellar ataxia type 3
Molecular Mechanisms of Neuroprotection in Polyglutamine-Dependent Degeneration
Identification of novel genes that modulate ATXN3 abundance
Apoptosis-related genes BCL2, BAX, AND TP53 as biomarkers of Spinocerebellar ataxia type 3 (SCA3)
Exploring the therapeutic capacity of Aripiprazole and related compounds for Machado-Joseph disease
Identification of therapeutic compounds for Spinocerebellar Ataxia type 3
Aripiprazole as a therapy for Spinocerebellar Ataxia type 3
Identification of predisposing CNS-penetrant therapeutic compounds for Spinocerebellar Ataxia Type 3
Mechanisms of Polyglutamine Neurodegeneration
Defining pathways that regulate levels of polyglutamine disease protein in MJD/SCA3
Unveiling pathways that regulate levels of polyglutamine disease protein in MJD/SCA3
Defining pathways that modulate levels of polyglutamine disease protein ATXN3 in MJD /SCA3
Developing a SCA3 Therapeutic: Small Molecules that Reduce Levels of Mutant Ataxin-3
Development of Therapeutic Strategies for Machado-Joseph Disease
Study of the mouse homologue gene that causes Machado-Joseph Disease
