A5080933567- Alzheimer's disease research and treatments
- Parkinson's Disease Mechanisms and Treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Nuclear Receptors and Signaling
- S100 Proteins and Annexins
- Prenatal Substance Exposure Effects
- Drug Transport and Resistance Mechanisms
- Cholinesterase and Neurodegenerative Diseases
- Advanced Fluorescence Microscopy Techniques
- Cell Image Analysis Techniques
- Inflammatory mediators and NSAID effects
- Amyotrophic Lateral Sclerosis Research
- Tryptophan and brain disorders
- Neonatal and fetal brain pathology
- Neuroscience and Neuropharmacology Research
- Computational Drug Discovery Methods
- Adenosine and Purinergic Signaling
- Endoplasmic Reticulum Stress and Disease
- Ubiquitin and proteasome pathways
- Autophagy in Disease and Therapy
- Photoacoustic and Ultrasonic Imaging
- Neuropeptides and Animal Physiology
- Neurological disorders and treatments
- 14-3-3 protein interactions
- Biosensors and Analytical Detection
University of Houston
2014-2024
The University of Texas Health Science Center at Houston
2012
Mayo Clinic in Florida
2002-2009
Jacksonville College
2002-2009
WinnMed
2004-2009
University of Massachusetts Amherst
2009
Mayo Clinic
2001-2007
Loyola University Chicago
1997-2003
Epidemiologic studies demonstrate that long-term use of NSAIDs is associated with a reduced risk for the development Alzheimer disease (AD). In this study, 20 commonly used NSAIDs, dapsone, and enantiomers flurbiprofen were analyzed their ability to lower level 42-amino-acid form amyloid beta protein (Abeta42) in human H4 cell line. Thirteen then tested acute dosing precursor (APP) transgenic mice, plasma brain levels Abeta drug evaluated. These show (a). eight FDA-approved Abeta42 vivo,...
Loss-of-function mutations in progranulin (GRN) cause ubiquitin- and TAR DNA-binding protein 43 (TDP-43)-positive frontotemporal dementia (FTLD-U), a progressive neurodegenerative disease affecting ∼10% of early-onset patients. Here we expand the role GRN FTLD-U demonstrate that common genetic variant (rs5848), located 3′-untranslated region (UTR) binding-site for miR-659, is major susceptibility factor FTLD-U. In series pathologically confirmed patients without mutations, show carriers...
Chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with a lower risk developing Alzheimer's disease. Recent evidence indicates that some NSAIDs specifically inhibit secretion the amyloidogenic Aβ42 peptide in cultured cells and mouse models The reduction peptides not mediated by inhibition cyclooxygenases (COX) but molecular mechanism underlying this novel activity has been further defined. We now demonstrate efficiently reduce intracellular pool cell-based studies...
An orally bioavailable and blood-brain barrier penetrating analog of the kinase inhibitor K252a was able to prevent typical motor deficits in tau (P301L) transgenic mouse model (JNPL3) markedly reduce soluble aggregated hyperphosphorylated tau. However, neurofibrillary tangle counts were not reduced successfully treated cohort, suggesting that main cytotoxic effects are exerted by tangles but lower molecular mass aggregates Our findings strongly suggest abnormal hyperphosphorylation plays a...
Epidemiologic studies demonstrate that long-term use of NSAIDs is associated with a reduced risk for the development Alzheimer disease (AD). In this study, 20 commonly used NSAIDs, dapsone, and enantiomers flurbiprofen were analyzed their ability to lower level 42-amino-acid form amyloid β protein (Aβ42) in human H4 cell line. Thirteen then tested acute dosing precursor (APP) transgenic mice, plasma brain levels Aβ drug evaluated. These show (a) eight FDA-approved Aβ42 vivo, (b) an NSAID...
Long-term use of non-steroidal anti-inflammatory drugs (NSAIDs) is associated with a reduced incidence Alzheimer's disease (AD). We and others have shown that certain NSAIDs reduce secretion Abeta42 in cell culture animal models, the effect on independent inhibition cyclooxygenase by these compounds. Since hypothesized to be initiating pathologic molecule AD, ability compounds lower selectively may their protective effect. previously identified R-flurbiprofen (tarenflurbil) as selective...
Alzheimer’s disease (AD) is a neurodegenerative disorder that characterized by progressive memory loss. In contrast, accumulating evidence suggests neuroprotective role of regular exercise in aging associated impairment. this study, we investigated the ability to prevent impairments short-term (STM) and early long-term potentiation (E-LTP) area CA1 hippocampus rat model AD (i.c.v. infusion 250 pmol/day Aβ1-42 peptides). We utilized behavioral assessment, vivo electrophysiological recording,...
Recent epidemiological evidence suggests that modifying lifestyle by increasing physical activity could be a non-pharmacological approach to improving symptoms and slowing disease progression in Alzheimer's other tauopathies. Previous studies have shown exercise reduces tau hyperphosphorylation, however, it is not known whether the accumulation of soluble or insoluble aggregates neurofibrillary tangles, which are both neuropathological hallmarks neurodegenerative tauopathy. In this study,...
In Alzheimer's disease (AD), a decline in explicit memory is one of the earliest signs and associated with hippocampal dysfunction. Amyloid protein exerts disruptive impact on neuronal function, but specific effects network activity are not well known. this study, fast voltage-sensitive dye imaging extracellular whole-cell electrophysiology were used entorhinal cortical-hippocampal slice preparations to characterize 12-16 month old female APPswe/PSEN1DeltaE9 (APdE9 mice) mice. Aged APdE9...
Epidemiological studies indicate that long term use of nonsteroidal anti-inflammatory drugs (NSAIDs) confers protection from Alzheimer's disease, and some NSAIDs were shown to specifically decrease production the amyloidogenic Aβ42 peptide, most likely by direct modulation γ-secretase activity. In contrast inhibitors, Aβ42-lowering do not impair S3 cleavage in NOTCH receptor release intracellular domain, a finding with conceptual implications for development safer targeting Aβ through...
Extracellular amyloid-β (Aβ) plaques and intracellular neurofibrillary tangles constitute the major neuropathological hallmarks of Alzheimer’s disease (AD). It is now apparent that parenchymal Aβ plaque deposition precedes behavioral signs by several years. The development agents can target these may be useful as diagnostic or therapeutic tools. In this study, we synthesized an Aβ-targeted lipid conjugate, incorporated it in stealth liposomal nanoparticles tested their ability to bind...
Section:ChooseTop of pageAbstract <<Materials and MethodsResultsDiscussionReferencesCITING ARTICLES