A5086318559- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Cholinesterase and Neurodegenerative Diseases
- Computational Drug Discovery Methods
- Intracerebral and Subarachnoid Hemorrhage Research
- Immune Response and Inflammation
Hope Center for Neurological Disorders
2018-2021
Chronic activation of brain innate immunity is a prominent feature Alzheimer's disease (AD) and primary tauopathies. However, to what degree contributes neurodegeneration as compared with pathological protein-induced neurotoxicity, the requirement particular glial cell type in neurodegeneration, are still unclear. Here we demonstrate that microglia-mediated damage, rather than tau-induced direct leading force driving tauopathy mouse model. Importantly, progression ptau pathology also driven...
The ε4 allele of the apolipoprotein E (APOE) gene is strongest genetic risk factor for late-onset Alzheimer's disease (AD) and greatly influences development amyloid-β (Aβ) pathology. Our current study investigated potential therapeutic effects anti-human APOE antibody HAE-4, which selectively recognizes human that co-deposited with Aβ in cerebral amyloid angiopathy (CAA) parenchymal In addition, we tested whether HAE-4 provoked brain hemorrhages, a component amyloid-related imaging...
The apolipoprotein E E4 allele of the APOE gene is strongest genetic factor for late-onset Alzheimer disease (LOAD). There compelling evidence that apoE influences (AD) in large part by affecting amyloid β (Aβ) aggregation and clearance; however, molecular mechanism underlying these findings remains largely unknown. Herein, we tested whether anti–human antibodies can decrease Aβ pathology mice producing both human apoE4, investigated effects. We utilized APPPS1-21 crossed to apoE4-knockin...