Publications
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September 25, 2020
pS421 huntingtin modulates mitochondrial phenotypes and confers neuroprotection in an HD hiPSC model
Huntington disease (HD), a devastating hereditary neurodegenerative disorder, is caused by an expansion of a CAG trinucleotide repeat that encodes a polyglutamine (polyQ) tract in the huntingtin (HTT) gene.
Journal: Cell Death & Disease
May 21, 2018
Large-scale transcriptomic analysis reveals that pridopidine reverses aberrant gene expression and activates neuroprotective pathways in the YAC128 HD mouse
Huntington Disease (HD) is an incurable autosomal dominant neurodegenerative disorder driven by an expansion repeat giving rise to the mutant huntingtin protein (mHtt), which is known to disrupt a multitude…
Journal: Molecular Neurodegeneration
December 7, 2017
Early pridopidine treatment improves behavioral and transcriptional deficits in YAC128 Huntington disease mice
Pridopidine is currently under clinical development for Huntington disease (HD), with on-going studies to better characterize its therapeutic benefit and mode of action. Pridopidine was administered either prior to the…
Journal: JCI Insight
November 23, 2017
Compositional differences between Copaxone and Glatopa are reflected in altered immunomodulation ex vivo in a mouse model.
Copaxone (glatiramer acetate, GA), a structurally and compositionally complex polypeptide nonbiological drug, is an effective treatment for multiple sclerosis, with a well-established favorable safety profile. The short antigenic polypeptide sequences…
Journal: Annals of the New York Academy of Sciences
May 31, 2017
A pharmacogenetic signature of high response to Copaxone in late-phase clinical-trial cohorts of multiple sclerosis
Copaxone is an efficacious and safe therapy that has demonstrated clinical benefit for over two decades in patients with relapsing forms of multiple sclerosis (MS). On an individual level, patients…
Journal: Genome Medicine
May 1, 2017
Pharmacogenomics strategies to optimize treatments for multiple sclerosis: Insights from clinical research.
Multiple sclerosis (MS) is a chronic, progressive, disabling disorder characterized by immune-mediated demyelination, inflammation, and neurodegenerative tissue damage in the central nervous system (CNS), associated with frequent exacerbations and remissions…
Journal: Progress in Neurobiology
November 3, 2016
The sigma-1 receptor mediates the beneficial effects of pridopidine in a mouse model of Huntington disease
The tri-nucleotide repeat expansion underlying Huntington disease (HD) results in corticostriatal synaptic dysfunction and subsequent neurodegeneration of striatal medium spiny neurons (MSNs). HD is a devastating autosomal dominant disease with…
Journal: Neurobiology of Disease
September 26, 2016
Laquinimod arrests experimental autoimmune encephalomyelitis by activating the aryl hydrocarbon receptor
Abstract Laquinimod is an oral drug currently being evaluated for the treatment of relapsing, remitting, and primary progressive multiple sclerosis and Huntington’s disease. Laquinimod exerts beneficial activities on both the…
Journal: Proceeding of the National Academy of Science
July 27, 2016
Pridopidine activates neuroprotective pathways impaired in Huntington Disease
Pridopidine has demonstrated improvement in Huntington Disease (HD) motor symptoms as measured by secondary endpoints in clinical trials. Originally described as a dopamine stabilizer, this mechanism is insufficient to explain…
Journal: Human Molecular Genetics
November 24, 2015
Functional effects of the antigen glatiramer acetate are complex and tightly associated with its composition
Glatiramer acetate (Copaxone®; GA) is a non-biological complex drug for multiple sclerosis. GA modulated thousands of genes in genome-wide expression studies conducted in THP-1 cells and mouse splenocytes. Comparing GA…
Journal: Journal of Neuroimmunology
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