about
New Therapeutic Strategies and Drug Candidates for Neurodegenerative Diseases: p53 and TNF- Inhibitors, and GLP-1 Receptor AgonistsBeta-Amyloid Precursor Protein (βAPP) Processing in Alzheimer's Disease (AD) and Age-Related Macular Degeneration (AMD)Alzheimer's disease beta-amyloid peptide is increased in mice deficient in endothelin-converting enzymeDifferential expression of cholesterol hydroxylases in Alzheimer's diseaseSelective butyrylcholinesterase inhibition elevates brain acetylcholine, augments learning and lowers Alzheimer beta-amyloid peptide in rodentSynthesis of the Alzheimer drug Posiphen into its primary metabolic products (+)-N1-norPosiphen, (+)-N8-norPosiphen and (+)-N1, N8-bisnorPosiphen, their inhibition of amyloid precursor protein, α-Synuclein synthesis, interleukin-1β release, and cholCharacterization of recombinant, soluble beta-secretase from an insect cell expression system.The Psen1-L166P-knock-in mutation leads to amyloid deposition in human wild-type amyloid precursor protein YAC transgenic mice.A novel endogenous indole protects rodent mitochondria and extends rotifer lifespan.Higher incidence of mild cognitive impairment in familial hypercholesterolemia.Geranylgeranyl pyrophosphate stimulates gamma-secretase to increase the generation of Abeta and APP-CTFgamma.Beta-secretase: structure, function, and evolution.Challenges associated with metal chelation therapy in Alzheimer's diseaseNeuronutrition and Alzheimer's diseaseGLP-1 receptor stimulation reduces amyloid-beta peptide accumulation and cytotoxicity in cellular and animal models of Alzheimer's disease.Incretin mimetics as pharmacologic tools to elucidate and as a new drug strategy to treat traumatic brain injuryResolution of inflammation is altered in Alzheimer's diseaseTargets for AD treatment: conflicting messages from γ-secretase inhibitorsAmyloid-beta peptide levels in brain are inversely correlated with insulysin activity levels in vivoEvidence of a novel mechanism for partial γ-secretase inhibition induced paradoxical increase in secreted amyloid β proteinCholesterol and Alzheimer's disease: clinical and experimental models suggest interactions of different genetic, dietary and environmental risk factors.Rationale for the development of cholinesterase inhibitors as anti-Alzheimer agents.Differential accumulation of secreted AbetaPP metabolites in ocular fluidsA partial failure of membrane protein turnover may cause Alzheimer's disease: a new hypothesis.Taking down the unindicted co-conspirators of amyloid beta-peptide-mediated neuronal death: shared gene regulation of BACE1 and APP genes interacting with CREB, Fe65 and YY1 transcription factors.Amyloid-beta protein clearance and degradation (ABCD) pathways and their role in Alzheimer's disease.Early-life events may trigger biochemical pathways for Alzheimer's disease: the "LEARn" model.TNF-alpha inhibition as a treatment strategy for neurodegenerative disorders: new drug candidates and targets.Role of DNA dynamics in Alzheimer's disease.Pigment epithelium-derived factor maintains retinal pigment epithelium function by inhibiting vascular endothelial growth factor-R2 signaling through gamma-secretaseSequence context effects in DNA replication blocks induced by aflatoxin B1Applying epigenetics to Alzheimer's disease via the latent early-life associated regulation (LEARn) model.Human retinal pigment epithelium cells as functional models for the RPE in vivo.Insulysin cleaves the APP cytoplasmic fragment at multiple sites.The experimental Alzheimer's disease drug posiphen [(+)-phenserine] lowers amyloid-beta peptide levels in cell culture and mice.Antisense-induced reduction of presenilin 1 expression selectively increases the production of amyloid beta42 in transfected cells.The heat shock/oxidative stress connection. Relevance to Alzheimer disease.The secretion of amyloid beta-peptides is inhibited in the tacrine-treated human neuroblastoma cells.Evidence for lymphatic Aβ clearance in Alzheimer's transgenic mice.Age-dependent loss of NGF signaling in the rat basal forebrain is due to disrupted MAPK activation
P50
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P50
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researcher
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wetenschapper
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հետազոտող
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K Sambamurti
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K Sambamurti
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K Sambamurti
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Kumar Sambamurti
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K Sambamurti
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K Sambamurti
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K Sambamurti
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Kumar Sambamurti
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K Sambamurti
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K Sambamurti
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K Sambamurti
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K Sambamurti
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Kumar Sambamurti
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P1053
A-1620-2012
P106
P1153
7003591212
P2798
P31
P496
0000-0001-9507-9214