A5006432058- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Cancer, Stress, Anesthesia, and Immune Response
- Neurogenesis and neuroplasticity mechanisms
- Neuropeptides and Animal Physiology
- Neuroscience and Neuropharmacology Research
- Tryptophan and brain disorders
- MicroRNA in disease regulation
- Bioinformatics and Genomic Networks
- Circadian rhythm and melatonin
- Amyotrophic Lateral Sclerosis Research
- Immune Cell Function and Interaction
- Neuroscience and Neural Engineering
- Receptor Mechanisms and Signaling
- Axon Guidance and Neuronal Signaling
- Health, Environment, Cognitive Aging
- Nutrition, Genetics, and Disease
- Neurogenetic and Muscular Disorders Research
- Parkinson's Disease Mechanisms and Treatments
- Cell Image Analysis Techniques
- Peroxisome Proliferator-Activated Receptors
- Helicobacter pylori-related gastroenterology studies
- Inflammation biomarkers and pathways
- 14-3-3 protein interactions
The University of Texas at Austin
2024
Washington University in St. Louis
2013-2023
Hope Center for Neurological Disorders
2021
Saint Louis University
2009-2010
Baoshan College
2010
Circadian dysfunction is a common attribute of many neurodegenerative diseases, most which are associated with neuroinflammation. rhythm has been inflammation in the periphery, but role core clock neuroinflammation remains poorly understood. Here we demonstrate that Rev-erbα, nuclear receptor and circadian component, mediator microglial activation We observed time-of-day oscillation immunoreactivity hippocampus, was disrupted Rev-erbα −/− mice. deletion caused spontaneous hippocampus...
Late onset Alzheimer's disease (LOAD) is a genetically complex and clinically heterogeneous disease. Recent large-scale genome wide association studies (GWAS) have identified more than twenty loci that modify risk for AD. Despite the identification of these loci, little progress has been made in identifying functional variants explain with AD risk. Thus, we sought to determine whether novel LOAD GWAS single nucleotide polymorphisms (SNPs) alter expression genes altered brains. The majority...
Significance Alzheimer’s disease (AD) remains a significant health burden within the aging population and currently lacks therapies that effectively target pathological events to halt development or progression of AD. The gene TREM2 appears influence abnormal protein accumulations in AD through brain’s immune cells; however, it is not clear if when might be targeted limit pathology response. We used antisense oligonucleotides (ASOs) reduce Trem2 levels mouse brain at specific times...
The protein tau and its isoforms are associated with several neurodegenerative diseases, many of which characterized by greater deposition the 4-repeat (4R) isoform; however, role 4R in disease pathogenesis remains unclear. We created antisense oligonucleotides (ASOs) that alter ratio 3R to investigate specific disease. Preferential expression human tau-expressing (hTau-expressing) mice was previously shown increase seizure severity phosphorylated without neuronal or synaptic loss. In this...
As embryonic stem cell-derived neural progenitors (NPs) have the potential to be used in cell replacement therapy, an understanding of signaling mechanisms that regulate their terminal differentiation is imperative. In previous studies, we discovered presence functional mu opioid receptors (MOR) and kappa (KOR) mouse cells NPs. Here, MOR KOR immunoreactivity was detected NP-derived oligodendrocytes during three stages maturation vitro. Moreover, examined modulation retinoic acid-induced NP...
Alzheimer's disease (AD) is characterized by the accumulation of amyloid-β (Aβ) in brain. Rare mutations APP, PSEN1, and PSEN2 have contributed to our understanding APP processing AD pathogenesis. APOE4 a major risk factor for late onset (LOAD) that produces genotype-specific differences Aβ clearance rates, illustrating value studying variants understand We recently identified several coding phospholipase D3 (PLD3) gene double LOAD. While normal function PLD3 poorly understood, highly...
Tauopathies are a class of neurodegenerative diseases that characterized by hyperphosphorylated tau aggregates in the brain. In subset tauopathies, genetic changes MAPT, gene encoding protein, sufficient to initiate cascade events leads aggregation and death neuronal populations Increasing evidence suggests spread along networks brain via release uptake. However, disease remains poorly understood. We sought develop stem cell model tauopathies captures complexities MAPT phenotypic human...
Abstract Background Select primary tauopathies exhibit MAPT (tau) mis‐splicing to produce an imbalance of 3R and 4R tau isoforms. Further, isoforms deposit in neurons glia tauopathy patients, although it remains unclear whether isoform deposition is a cause or consequence disease. Our group others have identified role for increased phosphorylation aggregation, suggesting that tau‐mediated mechanisms may influence Therefore, therapeutic strategies targeted against be beneficial. Method We...