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Inhibition of amyloid-beta aggregation by phenyl butyric acid analogs and bile acids: a comprehensive in silico study.
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Department of Biophysics, Panjab University, Chandigarh, 160014, India.
Alzheimer's disease (AD) is a degenerative neurological disorder defined by the formation of β-amyloid (Aβ) plaques and neurofibrillary tangles within the brain. Current pharmacological treatments for AD only provide symptomatic relief, and there is a lack of definitive disease-modifying therapies. Chemical chaperones, such as 4-Phenylbutyric acid (4PBA) and Tauroursodeoxycholic acid, have shown neuroprotective effects in animal and cell culture models.
View Article and Find Full Text PDFConfined active area and aggregation kinetic-based AuNPs@PVP nanosensors for simultaneous colorimetric detection of cysteine and homocysteine as homologues in human urine and serum.
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College of Chemistry, Chemical Engineering & Environmental Science, Minnan Normal University, Zhangzhou, 363000, China.
The detection of cysteine (Cys) and homocysteine (Hcy) in biological fluids has great significance for early diagnosis, including Alzheimer's and Parkinson's disease. The simultaneous determination of Cys and Hcy with a single probe is still a huge challenge. To enlarge the differences in space structure (line and ring) and energy (-721.
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NIHR Applied Research Collaboration Northwest London, London W12 0BZ, UK.
Mapping of Amyloid-β Aggregates In Vivo by a Fluorescent Probe with Dual Recognition Moieties.
Anal Chem
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State Key Laboratory of Chemical Resource Engineering, College of Chemistry, Beijing University of Chemical Technology, Beijing 100029, China.
The spontaneous aggregation of amyloid-β (Aβ) leads to neuronal cell death in the brain and causes the development of Alzheimer's disease (AD). The efficient detection of the aggregation state of Aβ holds significant promise for the early diagnosis and subsequent treatment of this neurodegenerative disorder. Currently, most of the fluorescent probes used for the detection of Aβ fibrils share similar recognition moieties, such as the ,-dimethylamino group, ,-diethylamino group, and piperidyl group.
View Article and Find Full Text PDFLow-dose intranasal deferoxamine modulates memory, neuroinflammation, and the neuronal transcriptome in the streptozotocin rodent model of Alzheimer's disease.
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HealthPartners Institute, Neuroscience Research, HealthPartners Neuroscience Center, Saint Paul, MN, United States.
Introduction: Intranasal (IN) deferoxamine (DFO) has emerged over the past decade as a promising therapeutic in preclinical experiments across neurodegenerative and neurovascular diseases. As an antioxidant iron chelator, its mechanisms are multimodal, involving the binding of brain iron and the consequent engagement of several pathways to counter pathogenesis across multiple diseases. We and other research groups have shown that IN DFO rescues cognitive impairment in several rodent models of Alzheimer Disease (AD).
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