Joseph Goodliffe

Joseph Goodliffe
Boston University | BU · Department of Anatomy and Neurobiology

Doctor of Philosophy

About

7
Publications
1,032
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205
Citations

Publications

Publications (7)
Article
Full-text available
In the BACHD mouse model of Huntington’s disease (HD), deletion of the N17 domain of the Huntingtin gene (BACHDΔN17, Q97) has been reported to lead to nuclear accumulation of mHTT and exacerbation of motor deficits, neuroinflammation and striatal atrophy (Gu et al., 2015). Here we characterized the effect of N17 deletion on dorsolateral striatal me...
Article
Functional recovery after cortical injury, such as stroke, is associated with neural circuit reorganization, but the underlying mechanisms and efficacy of therapeutic interventions promoting neural plasticity in primates are not well understood. Bone marrow mesenchymal stem cell-derived extracellular vesicles (MSC-EVs), which mediate cell-to-cell i...
Article
Full-text available
Huntington’s Disease (HD) is an autosomal dominant, progressive neurodegenerative disorder caused by deleterious expansion of CAG repeats in the Huntingtin gene and production of neurotoxic mutant Huntingtin protein (mHTT). The key pathological feature of HD is a profound degeneration of the striatum and a loss of cortical volume. The initial loss...
Data
Immunohistochemical validation of Vglut1 and Vglut2 antibodies. Images of immunohistochemical controls for Vglut1 and Vglut2 shown in the absence (a, Vglut1; c, Vglut2) or presence (b, Vglut1; d, Vglut2) of primary antibody. Antibody specificity was validated by antibody reabsorption with control protein to Vglut1 and Vglut2 (e, Vglut1 antibody, Vg...
Data
Physiological and morphological properties of WT D1 vs. WT D2 MSNs. (DOCX)
Article
Full-text available
Studies in humans with Down syndrome (DS) show that alterations in fetal brain development are followed by postnatal deficits in neuronal numbers, synaptic plasticity, and cognitive and motor function. This same progression is replicated in several mouse models of DS. Dp(16)1Yey/+ (hereafter called Dp16) is a recently developed mouse model of DS in...
Article
Trisomy 21, or Down syndrome (DS), is the most common genetic cause of developmental delay and intellectual disability. To gain insight into the underlying molecular and cellular pathogenesis, we conducted a multi-region transcriptome analysis of DS and euploid control brains spanning from mid-fetal development to adulthood. We found genome-wide al...

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