A5080782448- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Curcumin's Biomedical Applications
- Fatty Acid Research and Health
- Cholinesterase and Neurodegenerative Diseases
- Nuclear Receptors and Signaling
- Neuroscience and Neuropharmacology Research
- Prion Diseases and Protein Misfolding
- S100 Proteins and Annexins
- Cholesterol and Lipid Metabolism
- Peroxisome Proliferator-Activated Receptors
- Neurological Disease Mechanisms and Treatments
- Computational Drug Discovery Methods
- Tryptophan and brain disorders
- Mitochondrial Function and Pathology
- Dementia and Cognitive Impairment Research
- Biochemical effects in animals
- 14-3-3 protein interactions
- Natural Antidiabetic Agents Studies
- Fibroblast Growth Factor Research
- Nicotinic Acetylcholine Receptors Study
- Bone Metabolism and Diseases
- Eicosanoids and Hypertension Pharmacology
- Parkinson's Disease Mechanisms and Treatments
- Nerve injury and regeneration
University of California, Los Angeles
2015-2025
VA Greater Los Angeles Healthcare System
2015-2025
Geriatric Research Education and Clinical Center
2011-2025
Invision Sally Jobe
2021
Foundation for Psychocultural Research
2012-2019
University of Illinois Chicago
2016
Los Angeles Medical Center
2012-2013
West Los Angeles College
2013
UCLA Health
2008-2012
Cedars-Sinai Medical Center
2010
Alzheimer's disease (AD) involves amyloid β (Aβ) accumulation, oxidative damage, and inflammation, risk is reduced with increased antioxidant anti-inflammatory consumption. The phenolic yellow curry pigment curcumin has potent activities can suppress cognitive deficits, accumulation. Since the molecular structure of suggested potential Aβ binding, we investigated whether its efficacy in AD models could be explained by effects on aggregation. Under aggregating conditions vitro, inhibited...
Inflammation in Alzheimer9s disease (AD) patients is characterized by increased cytokines and activated microglia. Epidemiological studies suggest reduced AD risk associates with long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs). Whereas chronic ibuprofen suppressed inflammation plaque-related pathology an Alzheimer transgenic APPSw mouse model (Tg2576), excessive NSAIDs targeting cyclooxygenase I can cause gastrointestinal, liver, renal toxicity. One alternative NSAID curcumin,...
The brain in Alzheimer's disease (AD) shows a chronic inflammatory response characterized by activated glial cells and increased expression of cytokines complement factors surrounding amyloid deposits. Several epidemiological studies have demonstrated reduced risk for AD patients using nonsteroidal anti-inflammatory drugs (NSAIDs), prompting further inquiries about how NSAIDs might influence the development pathology inflammation CNS. We tested impact orally administered ibuprofen, most...
Epidemiological studies suggest that increased intake of the omega-3 (n-3) polyunsaturated fatty acid (PUFA) docosahexaenoic (DHA) is associated with reduced risk Alzheimer's disease (AD). DHA levels are lower in serum and brains AD patients, which could result from low dietary and/or PUFA oxidation. Because effects on Alzheimer pathogenesis, particularly amyloidosis, unknown, we used APPsw (Tg2576) transgenic mouse model to evaluate impact amyloid precursor protein (APP) processing burden....
Curcumin can reduce inflammation and neurodegeneration, but its chemical instability metabolism raise concerns, including whether the more stable metabolite tetrahydrocurcumin (TC) may mediate efficacy. We examined antioxidant, anti-inflammatory, or anti-amyloidogenic effects of dietary curcumin TC, either administered chronically to aged Tg2576 APP<i>sw</i> mice acutely lipopolysaccharide (LPS)-injected wild-type mice. Despite dramatically higher drug plasma levels after TC compared with...
Both insulin resistance (type II diabetes) and β-amyloid (Aβ) oligomers are implicated in Alzheimer9s disease (AD). Here, we investigate the role of Aβ oligomer-induced c-Jun N-terminal kinase (JNK) activation leading to phosphorylation degradation adaptor protein receptor substrate-1 (IRS-1). IRS-1 couples other trophic factor receptors downstream kinases neuroprotective signaling. Increased phospho-IRS-1 is found AD brain insulin-resistant tissues from diabetics. report significantly...
Curcumin is a polyphenolic compound derived from the plant Curcuma Long Lin that has been demonstrated to have antioxidant and anti-inflammatory effects as well on reducing beta-amyloid aggregation. It reduces pathology in transgenic models of Alzheimer's disease (AD) promising candidate for treating human AD. The purpose current study generate tolerability preliminary clinical biomarker efficacy data curcumin persons with AD.We performed 24-week randomized, double blind, placebo-controlled...
Noninvasive detection of Alzheimer's disease (AD) with high specificity and sensitivity can greatly facilitate identification at-risk populations for earlier, more effective intervention. AD patients exhibit a myriad retinal pathologies, including hallmark amyloid β-protein (Aβ) deposits.Burden, distribution, cellular layer, structure Aβ plaques were analyzed in flat mounts cross sections definite controls (n = 37). In proof-of-concept imaging trial 16), probe curcumin formulation was...
Insulin-degrading enzyme (IDE) is one of the proteins that has been demonstrated to play a key role in degrading β-amyloid (Aβ) monomer vitro and vivo , raising possibility upregulating IDE as an approach reduce Aβ. Little known, however, about cellular molecular regulation protein. Because main functions degrade insulin, we hypothesized there negative feedback mechanism whereby stimulation insulin receptor-mediated signaling upregulates prevent chronic activation pathway. We show treatment...
Abstract In the central nervous system (CNS), nerve regeneration after traumatic injury fails. The formation of a dense fibrous scar is thought to restrict in part growth axonal projections, providing one many reasons that complete lesions neural pathways adult mammalian CNS are rarely followed by significant functional recovery. order determine which mechanisms mediate and investigate whether they can be modulated vivo , we have attempted define potential role trophic factors. Our previous...
Traumatic injury to the CNS initiates transient and unsuccessful regeneration of damaged neural pathways, accompanied by reactive gliosis, angiogenesis, deposition a dense fibrous glial/meningeal scar at wound site. Basic fibroblast growth factor (basic FGF) is protein with potent effects on neurons, glia, fibroblasts, vascular endothelial cells. Hybridization immunocytochemical methods were used examine temporal spatial changes in distribution levels basic FGF mRNA also its receptor (flg),...
Although amyloid deposits have long been known to accumulate in Alzheimer disease (AD) brain, their origin and significance remain speculative. Because of the lack an vivo model where can be induced, relationship extracellular beta-amyloid other AD pathology has never directly investigated. Therefore, we injected SDS-isolated cores into rat cortex hippocampus. Similarly isolated lipofuscin fractions from control human brains were on contralateral side. Rats perfused examined...
Abstract Epidemiological data indicate that low n‐3 polyunsaturated fatty acids (PFA) intake is a readily manipulated dietary risk factor for Alzheimer's disease (AD). Studies in animals confirm the deleterious effect of PFA depletion on cognition and dendritic scaffold proteins. Here, we show transgenic mice overexpressing human AD gene APPswe (Tg2576), safflower oil‐induced deficiency caused decrease N ‐methyl‐ d ‐aspartate (NMDA) receptor subunits, NR2A NR2B, cortex hippocampus with no...