Cassandra L. Rosenberg
A5033286359- Neuroinflammation and Neurodegeneration Mechanisms
- Alzheimer's disease research and treatments
- Inflammation biomarkers and pathways
- Dementia and Cognitive Impairment Research
- Apelin-related biomedical research
- Macrophage Migration Inhibitory Factor
- Medicinal Plants and Neuroprotection
- Cholesterol and Lipid Metabolism
- Natural Antidiabetic Agents Studies
- Immune cells in cancer
- Parkinson's Disease Mechanisms and Treatments
Mayo Clinic in Florida
2021-2024
Apolipoprotein E (APOE) genetic variants have been shown to modify Alzheimer’s disease (AD) risk. We previously identified an APOE3 variant (APOE3-V236E), named APOE3-Jacksonville (APOE3-Jac), associated with healthy brain aging and reduced risk for AD dementia Lewy bodies (DLB). Herein, we resolved the functional mechanism by which APOE3-Jac reduces APOE aggregation enhances its lipidation in human brains, as well cellular biochemical assays. Compared APOE3, expression of astrocytes...
Abstract Background Abnormal lipid accumulation has been recognized as a key element of immune dysregulation in microglia whose dysfunction contributes to neurodegenerative diseases. Microglia play essential roles the clearance lipid-rich cellular debris upon myelin damage or demyelination, common pathogenic event neuronal disorders. Apolipoprotein E (apoE) plays pivotal role brain homeostasis; however, apoE isoform-dependent mechanisms regulating microglial response demyelination remain...
Abstract Background The rare p.H157Y variant of TREM2 (Triggering Receptor Expressed on Myeloid Cells 2) was found to increase Alzheimer’s disease (AD) risk. This mutation is located at the cleavage site extracellular domain. Ectopic expression TREM2-H157Y in HEK293 cells resulted increased shedding. However, physiological outcomes H157Y remain unknown absence and presence AD related pathologies. Methods We generated a novel Trem2 knock-in mouse model through CRISPR/Cas9 technology...
Abstract Alzheimer’s disease (AD), characterized by the deposition of amyloid-β (Aβ) in senile plaques and neurofibrillary tangles phosphorylated tau (pTau), is increasingly recognized as a complex with multiple pathologies. AD sometimes pathologically overlaps age-related tauopathies such four repeat (4R)-tau predominant argyrophilic grain (AGD). While AGD often detected pathology, contribution APOE4 to risk not clear despite its robust effects on pathogenesis. Specifically, how APOE...