A5085286332- Genetic Neurodegenerative Diseases
- Down syndrome and intellectual disability research
- Neurological disorders and treatments
- Mitochondrial Function and Pathology
- Congenital heart defects research
- Thermal Regulation in Medicine
- Neuroscience and Neuropharmacology Research
- Genomic variations and chromosomal abnormalities
- Reproductive Biology and Fertility
- Prenatal Screening and Diagnostics
- Genetics and Neurodevelopmental Disorders
- Sperm and Testicular Function
- Extracellular vesicles in disease
- Robotics and Automated Systems
- Neuroinflammation and Neurodegeneration Mechanisms
- RNA regulation and disease
Boston University
2016-2020
Institute of Neurobiology
2020
Studies in humans with Down syndrome (DS) show that alterations fetal brain development are followed by postnatal deficits neuronal numbers, synaptic plasticity, and cognitive motor function. This same progression is replicated several mouse models of DS. Dp(16)1Yey/+ (hereafter called Dp16) a recently developed model DS which the entire region chromosome 16 homologous to human 21 has been triplicated. As such, Dp16 mice may more closely reproduce neurodevelopmental changes occurring Here,...
Functional recovery after cortical injury, such as stroke, is associated with neural circuit reorganization, but the underlying mechanisms and efficacy of therapeutic interventions promoting plasticity in primates are not well understood. Bone marrow mesenchymal stem cell-derived extracellular vesicles (MSC-EVs), which mediate cell-to-cell inflammatory trophic signaling, thought be viable targets. We recently showed, aged female rhesus monkeys, that systemic administration MSC-EVs enhances...
Huntington's Disease (HD) is an autosomal dominant, progressive neurodegenerative disorder caused by deleterious expansion of CAG repeats in the Huntingtin gene and production neurotoxic mutant protein (mHTT). The key pathological feature HD a profound degeneration striatum loss cortical volume. initial indirect pathway (D2) medium spiny neuron (MSN) projections early stages HD, followed direct (D1) advanced has important implications for trajectory motor cognitive dysfunction but not yet...
In the BACHD mouse model of Huntington's disease (HD), deletion N17 domain Huntingtin gene (BACHDΔN17, Q97) has been reported to lead nuclear accumulation mHTT and exacerbation motor deficits, neuroinflammation striatal atrophy (Gu et al., 2015). Here we characterized effect on dorsolateral medium spiny neurons (MSNs) in BACHDΔN17 (Q97) BACWTΔN17 (Q31) mice by comparing them MSNs wildtype (WT) mice. Mice were a series tasks subsequently whole cell patch clamp recordings with simultaneous...