A5085826986- Alzheimer's disease research and treatments
- Microtubule and mitosis dynamics
- Neuroscience and Neuropharmacology Research
- Trace Elements in Health
- Cholinesterase and Neurodegenerative Diseases
- Chromosomal and Genetic Variations
- Axon Guidance and Neuronal Signaling
- Ion channel regulation and function
- Cancer-related Molecular Pathways
- Tryptophan and brain disorders
- 14-3-3 protein interactions
- Neuroinflammation and Neurodegeneration Mechanisms
- Advanced biosensing and bioanalysis techniques
The University of Texas Health Science Center at San Antonio
2020-2023
Institute for Neurodegenerative Disorders
2020-2023
The University of Texas MD Anderson Cancer Center
2021-2023
The University of Texas at San Antonio
2019-2023
Longevity Biotech (United States)
2020
Transposable elements comprise almost half of the mammalian genome. A growing body evidence suggests that transposable element dysregulation accompanies brain aging and neurodegenerative disorders, activation is neurotoxic. Recent studies have identified links between pathogenic forms tau, a protein accumulates in Alzheimer's disease related "tauopathies," element-induced neurotoxicity. Starting with transcriptomic analyses, we find age- tau-induced occurs mouse brain. Among are activated at...
Pervasive neuroinflammation occurs in many neurodegenerative diseases, including Alzheimer's disease (AD). SPI1/PU.1 is a transcription factor located at genome-wide significant AD-risk locus and its reduced expression associated with delayed onset of AD. We analyzed single-cell transcriptomic datasets from microglia human AD patients found an enrichment PU.1-binding motifs the differentially expressed genes. In hippocampal tissues transgenic mice neurodegeneration, we vastly increased...
In Alzheimer's disease, neurons acquire phenotypes that are also present in various cancers, including aberrant activation of the cell cycle. Unlike cancer, cycle post-mitotic is sufficient to induce death. Multiple lines evidence suggest abortive a consequence pathogenic forms tau, protein drives neurodegeneration disease and related "tauopathies." Here we combine network analyses human mouse models primary tauopathy with studies Drosophila discover tau drive by disrupting cellular program...
Synaptic activity-induced calcium (Ca2+) influx and subsequent propagation into the nucleus is a major way in which synapses communicate with to regulate transcriptional programs important for activity-dependent survival memory formation. Nuclear Ca2+ shapes transcriptome by regulating cyclic AMP (cAMP) response element-binding protein (CREB). Here, we utilize Drosophila model of tauopathy induced pluripotent stem cell (iPSC)-derived neurons from humans Alzheimer's disease study effects...
Synaptic activity-induced calcium ion (Ca2+) influx and subsequent propagation of Ca2+ into the nucleus is a major way in which synapses communicate with to regulate transcriptional programs that maintain activity-dependent survival mediate memory formation. Nuclear shapes transcriptome by regulating cAMP response element-binding protein (CREB)-dependent transcription. Here we utilize Drosophila induced pluripotent stem cell (iPSC)-derived neurons from humans Alzheimer's disease study...
Abstract Neurons in human Alzheimer’s disease acquire phenotypes that are also present various cancers, including over-stabilization of the cytoskeleton, nuclear pleomorphism, decondensation constitutive heterochromatin, and aberrant activation cell cycle. Unlike cancer, which cycle drives tumor formation, post-mitotic neurons is sufficient to induce neuronal death. Multiple lines evidence suggest abortive a consequence pathogenic forms tau, protein neurodegeneration related “tauopathies.”...
Abstract Alzheimer’s disease (AD) is an irreversible neurodegenerative disorder which characterized by neurofibrillary tau tangles and amyloid-ß plaques. Our laboratory uses transgenic Drosophila to rapidly test hypotheses along with human brain samples in order ensure that our work relevant clinical endeavors. Using this approach, we identified a pathway whereby pathological over-stabilizes filamentous actin (f-actin), leading disrupting aberrant nuclear pleomorphisms decondensation of...