A5032498766- Neuroinflammation and Neurodegeneration Mechanisms
- Phagocytosis and Immune Regulation
- Alzheimer's disease research and treatments
- Immune cells in cancer
- Congenital Heart Disease Studies
- Congenital heart defects research
- Cancer-related cognitive impairment studies
- Cholinesterase and Neurodegenerative Diseases
- Spaceflight effects on biology
- Tissue Engineering and Regenerative Medicine
- SARS-CoV-2 and COVID-19 Research
- Neurogenesis and neuroplasticity mechanisms
- Erythrocyte Function and Pathophysiology
- Atherosclerosis and Cardiovascular Diseases
- Galectins and Cancer Biology
- Endoplasmic Reticulum Stress and Disease
- Genetics, Aging, and Longevity in Model Organisms
University of Rochester
2019-2024
University of Rochester Medical Center
2020-2023
Abstract Background Neuroinflammation is thought to contribute the pathogenesis of Alzheimer’s disease (AD), yet numerous studies have demonstrated a beneficial role for neuroinflammation in amyloid plaque clearance. We previously shown that sustained expression IL-1β hippocampus APP/PS1 mice decreases burden independent recruited CCR2 + myeloid cells, suggesting resident microglia as main phagocytic effectors IL-1β-induced To date, however, mechanisms clearance remain poorly understood....
Alzheimer's disease is the leading cause of dementia worldwide. TAM receptor tyrosine kinases (Tyro3, Axl, MerTK) are known for their role in engagement phagocytosis and modulation inflammation, recent evidence suggests a complex relationship between Mer, microglial amyloid plaques AD. Gas6, primary CNS ligand, reduces neuroinflammation improves outcomes murine models disease. Therefore, we hypothesized that AAV-mediated overexpression Gas6 would alleviate plaque pathology, reduce...
Neuroinflammation driven by the accumulation of amyloid β (Aβ) can lead to neurofibrillary tangle formation in Alzheimer's Disease (AD). To test hypothesis that an anti-inflammatory immunomodulatory agent might have beneficial effects on and tau pathology, as well microglial phenotype, we evaluated glatiramer acetate (GA), a multiple sclerosis drug thought bias type 2 helper T (Th2) cell responses alternatively activate myeloid cells. We administered weekly subcutaneous injections GA or PBS...
Abstract Mutations in the TANGO2 gene cause severe illness humans, including life-threatening metabolic crises; however, function of protein remains unknown. In a recent publication Nature , Sun et al. proposed that helps transport haem within and between cells, from areas with high concentrations to those lower concentrations. Caenorhabditis elegans has two versions called HRG-9 HRG-10. They demonstrated worms deficient these proteins show increased survival upon exposure toxic analog,...
Abstract TANGO2 deficiency disorder (TDD) is a rare, autosomal recessive condition caused by pathogenic variants in , gene residing within the region commonly deleted 22q11.2 deletion syndrome (22q11.2DS). Although patients with 22q11.2DS are at substantially higher risk for comorbid TDD, it remains underdiagnosed 22q11.2DS, likely due to overlapping symptomatology and lack of knowledge about TDD. Initiation B‐vitamin supplementation may provide therapeutic benefit highlighting need...
Microglia, the resident immune cells of central nervous system (CNS), play multiple roles in maintaining CNS homeostasis and mediating tissue repair, including proliferating response to brain injury disease. Cranial irradiation (CI), used for treatment tumors, has a long-lasting anti-proliferative effect on number cell types brain, oligodendrocyte progenitor neural cells; however, CI CNS-resident microglial proliferation is not well characterized. Using sterile cortical needle stab model...
Abstract Background Microglia, the immune cells of brain, play seemingly antagonistic roles in Alzheimer’s disease (AD) brain. On one hand, microglia contribute to clearance amyloid beta (Aβ) plaques via phagocytosis. other activated produce inflammatory cytokines that a hostile neuronal environment, exacerbating AD pathogenesis. Axl, member TAM receptor family, is increased on surround Aβ plaques. Gas6, primary ligand for promotes phagocytosis and suppresses inflammation peripheral cells....
Abstract The phagocytosis of apoptotic cells and cellular debris by microglia critically regulates immune homeostasis in the brain. In Alzheimer’s Disease (AD), microglial amyloid-β (Aβ) aggregates is thought to play a protective role AD pathogenesis, but mechanisms which this occurs are not well understood. Recent work has suggested that phosphatidylserine (PtdSer)-sensing receptors may induce Aβ plaque engulfment, data from our lab others’ supports idea. To better understand PtdSer-sensing...
Abstract Background: Alzheimer’s disease is the leading cause of dementia worldwide. TAM receptor tyrosine kinases (Tyro3, Axl, MerTK) are known for their role in engagement phagocytosis and modulation inflammation, recent evidence suggests a complex relationship between Mer, microglial amyloid plaques AD. Gas6, primary CNS ligand, reduces neuroinflammation improves outcomes murine models disease. Therefore, we hypothesized that AAV-mediated overexpression Gas6 would alleviate plaque...