A5001725894- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Prion Diseases and Protein Misfolding
- Computational Drug Discovery Methods
- Cholinesterase and Neurodegenerative Diseases
- Immune Response and Inflammation
- DNA Repair Mechanisms
- Cytomegalovirus and herpesvirus research
- S100 Proteins and Annexins
- Nuclear Receptors and Signaling
- Drug Transport and Resistance Mechanisms
- Amyloidosis: Diagnosis, Treatment, Outcomes
- Biochemical and Molecular Research
- Nerve injury and regeneration
- Proteoglycans and glycosaminoglycans research
- Cholesterol and Lipid Metabolism
- Glycosylation and Glycoproteins Research
- Protein Structure and Dynamics
- Psoriasis: Treatment and Pathogenesis
- Phosphodiesterase function and regulation
- Pluripotent Stem Cells Research
- Neurogenesis and neuroplasticity mechanisms
- Tryptophan and brain disorders
- Biomedical Research and Pathophysiology
- Wnt/β-catenin signaling in development and cancer
University of Illinois Urbana-Champaign
2005-2023
Illinois College
2005-2023
University of Illinois Chicago
2007-2020
Saga University
2006
University of Alabama at Birmingham
1996-2005
Showa University
2001
University of Washington
1988-1995
University of Washington Medical Center
1989-1994
Alzheimer’s Disease Neuroimaging Initiative
1994
Osaka University
1990
Werner syndrome (WS) is a rare autosomal-recessive disorder characterized by the premature appearance of features normal aging in young adults. The extensive phenotypic overlap between WS and suggests they may also share pathogenetic mechanisms. We reported previously that somatic cells from patients demonstrate propensity to develop chromosomal aberrations, including translocations, inversions, deletions, cell lines high spontaneous mutation rate 6-thioguanine resistance. report here...
Amyloid plaques, a pathological hallmark of Alzheimer's disease (AD), are accompanied by activated microglia. The role microglia in the pathogenesis AD remains controversial: either clearing Aβ deposits phagocytosis or releasing proinflammatory cytokines and cytotoxic substances. Microglia can be via toll-like receptors (TLRs), class pattern-recognition innate immune system. We previously demonstrated that an mouse model homozygous for loss-of-function mutation TLR4 had increases...
The insoluble amyloid deposited extracellularly in the brains of patients with Alzheimer's disease (AD) is composed β protein, a ∼4-kDa secreted protein that derived from set large proteins collectively referred to as precursor (βAPP). During normal processing βAPP cleaved by secretase, producing NH2-terminal derivative (sAPPβ) and COOH-terminal fragment beginning at Aβ1, which subsequently γ secretase releasing Aβ. Most Aβ Aβ1-40, but ∼10% Aβ1-42. Alternative cleavage α produces slightly...
Accumulation of amyloid-β protein (Aβ) in the brain is thought to be a causal event Alzheimer's disease (AD). Immunotherapy targeting Aβ holds great promise for reducing brain. Here, we evaluated efficacy and safety anti-Aβ single