- Neuroinflammation and Neurodegeneration Mechanisms
- Alzheimer's disease research and treatments
- Gut microbiota and health
- Tryptophan and brain disorders
- Sleep and Wakefulness Research
- Neurological Disease Mechanisms and Treatments
- Inflammation biomarkers and pathways
- Cholesterol and Lipid Metabolism
- Sleep and related disorders
- Immune cells in cancer
- Cerebrovascular and genetic disorders
- Cerebrospinal fluid and hydrocephalus
- Intracerebral and Subarachnoid Hemorrhage Research
- Hormonal Regulation and Hypertension
Hope Center for Neurological Disorders
2022-2024
Washington University in St. Louis
2023-2024
University of Missouri–St. Louis
2023
Sleep loss is associated with cognitive decline in the aging population and a risk factor for Alzheimer’s disease (AD). Considering crucial role of immunomodulating genes such as that encoding triggering receptor expressed on myeloid cells type 2 (TREM2) removing pathogenic amyloid-β (Aβ) plaques regulating neurodegeneration brain, our aim was to investigate whether how sleep influences microglial function mice. We chronically sleep-deprived wild-type mice 5xFAD mouse model cerebral...
Abstract It has recently become well-established that there is a connection between Alzheimer’s disease pathology and gut microbiome dysbiosis. We have previously demonstrated antibiotic-mediated microbiota perturbations lead to attenuation of Aβ deposition, phosphorylated tau accumulation, disease-associated glial cell phenotypes in sex-dependent manner. In this regard, we were intrigued by the finding marine-derived oligosaccharide, GV-971, was reported alter reduce amyloidosis 5XFAD mouse...
Alzheimer's disease (AD) is the most common cause of dementia. The APOE-ε4 allele apolipoprotein E (APOE) gene strongest genetic risk factor for late-onset AD. APOE genotype modulates effect sleep disruption on AD risk, suggesting a possible link between apoE and in pathogenesis, which relatively unexplored. We hypothesized that modifies Aβ deposition plaque-associated tau seeding spreading form neuritic plaque-tau (NP-tau) pathology response to chronic deprivation (SD) an isoform-dependent...
Abstract Background Alzheimer Disease (AD) and cerebral amyloid angiopathy (CAA) are both characterized by amyloid-β (Aβ) accumulation in the brain, although Aβ deposits mostly brain parenchyma AD cerebrovasculature CAA. The presence of CAA can exacerbate clinical outcomes patients promoting spontaneous intracerebral hemorrhage ischemia leading to CAA-associated cognitive decline. Genetically, share ε4 allele apolipoprotein E ( APOE ) gene as strongest genetic risk factor. Although...
Parenchymal border macrophages (PBMs) reside close to the central nervous system parenchyma and regulate CSF flow dynamics. We recently demonstrated that PBMs provide a clearance pathway for amyloid-β peptide, which accumulates in brain Alzheimer’s disease (AD). Given emerging role AD, we explored how tau pathology affects PBM populations PS19 mouse model of pathology. reduction flow, an increase MHCII + subpopulation mice compared with WT littermates. Consequently, asked whether dysfunction...
Abstract Background Sleep disturbances are associated with the pathogenesis of neurodegenerative diseases including Alzheimer’s disease (AD) and primary tauopathies. We have previously shown that APOE4, strongest genetic risk factor for AD, directly influences severity key pathological hallmarks neurodegeneration tau deposition, microglial reactivity brain atrophy. loss accumulation in both mice humans, suggesting sleep may contribute to not only by influencing protein aggregation, but also...
Abstract It has recently become well-established that there is a connection between Alzheimer’s disease pathology and gut microbiome dysbiosis. We have previously demonstrated antibiotic-mediated microbiota perturbations lead to attenuation of Aβ deposition, phosphorylated tau accumulation, disease-associated glial cell phenotypes in sex-dependent manner. In this regard, we were intrigued by the finding marine-derived oligosaccharide, GV-971, was reported alter reduce amyloidosis mouse...