نتایج جستجو برای: β-amyloid peptide clearance

تعداد نتایج: 397200  

Journal: :avicenna journal of neuro psycho physiology 0
ali nikkhah neurophysiology research center, hamadan university of medical sciences, hamadan, ir iran fatemeh ghahremanitamadon neurophysiology research center, hamadan university of medical sciences, hamadan, ir iran somayeh zargooshnia neurophysiology research center, hamadan university of medical sciences, hamadan, ir iran siamak shahidi neurophysiology research center, hamadan university of medical sciences, hamadan, ir iran sara soleimani asl neurophysiology research center, hamadan university of medical sciences, hamadan, ir iran; department of anatomy, hamadan university of medical sciences, hamadan, ir iran; neurophysiology research center, hamadan university of medical sciences, hamadan, ir iran, tel/fax: +98-8118380208

conclusions these data suggest that single bilateral microinjection of aβ (25-35) could impair memory and can be used as an ad model in wistar rats. results the results showed that aβ (25-35) significantly impaired both step-through latency and time in dark compartment in the passive avoidance task. background alzheimer's disease (ad) is the most common form of dementia that leads to neurotoxic...

Journal: :iranian journal of pharmaceutical research 0
jalal pourahmad - mehrdad faizi department of pharmacology and toxicology, faculty of pharmacy, shahid beheshti university of medical sciences, p.o. box 14155-6153, tehran, iran. enayatollah seydi department of pharmacology and toxicology, faculty of pharmacy, shahid beheshti university of medical sciences, p.o. box 14155-6153, tehran, iran. sadegh abarghuyi faculty of pharmacy, shahid beheshti university of medical sciences, p.o. box 14155-6153, tehran, iran. ahmad salimi department of pharmacology and toxicology, faculty of pharmacy, shahid beheshti university of medical sciences, p.o. box 14155-6153, tehran, iran. sanaz nasoohi department of pharmacology and toxicology, faculty of pharmacy, shahid beheshti university of medical sciences, p.o. box 14155-6153, tehran, iran.

alzheimer’s disease (ad) is a progressive neurodegenerative disorder that affects regions of the brain that control cognition, memory, language, speech and awareness to one’s physical surroundings. the pathological initiation and progression of ad is highly complex and its prevalence is on the rise. in his study, alzheimer's disease was induced with single injection of amyloid-β (aβ) pepti...

2015
Claudia Späni Tobias Suter Rebecca Derungs Maria Teresa Ferretti Tobias Welt Fabian Wirth Christoph Gericke Roger M. Nitsch Luka Kulic

INTRODUCTION In Alzheimer's disease, accumulation and pathological aggregation of amyloid β-peptide is accompanied by the induction of complex immune responses, which have been attributed both beneficial and detrimental properties. Such responses implicate various cell types of the innate and adaptive arm of the immunesystem, both inside the central nervous system, and in the periphery. To inve...

Journal: :Brain : a journal of neurology 2011
Dun-Sheng Yang Philip Stavrides Panaiyur S Mohan Susmita Kaushik Asok Kumar Masuo Ohno Stephen D Schmidt Daniel Wesson Urmi Bandyopadhyay Ying Jiang Monika Pawlik Corrinne M Peterhoff Austin J Yang Donald A Wilson Peter St George-Hyslop David Westaway Paul M Mathews Efrat Levy Ana M Cuervo Ralph A Nixon

Autophagy, a major degradative pathway for proteins and organelles, is essential for survival of mature neurons. Extensive autophagic-lysosomal pathology in Alzheimer's disease brain contributes to Alzheimer's disease pathogenesis, although the underlying mechanisms are not well understood. Here, we identified and characterized marked intraneuronal amyloid-β peptide/amyloid and lysosomal system...

Journal: :Journal of Alzheimer's disease : JAD 2012
Bernd Bohrmann Karlheinz Baumann Jörg Benz Francoise Gerber Walter Huber Frédéric Knoflach Jürg Messer Krisztina Oroszlan Robert Rauchenberger Wolfgang F Richter Christine Rothe Margit Urban Michael Bardroff Michael Winter Christer Nordstedt Hansruedi Loetscher

The amyloid-β lowering capacity of anti-Aβ antibodies has been demonstrated in transgenic models of Alzheimer's disease (AD) and in AD patients. While the mechanism of immunotherapeutic amyloid-β removal is controversial, antibody-mediated sequestration of peripheral Aβ versus microglial phagocytic activity and disassembly of cerebral amyloid (or a combination thereof) has been proposed. For su...

Journal: :Journal of neurochemistry 2012
Julien Delrieu Pierre Jean Ousset Céline Caillaud Bruno Vellas

Recent advances in the understanding of Alzheimer's disease pathogenesis have led to the development of numerous compounds that might modify the disease process. Amyloid β (Aβ) peptide represents an important molecular target for intervention in Alzheimer's disease. Several types of Aβ peptide immunotherapy for Alzheimer's disease are under investigation, direct immunization with synthetic inta...

Interactions of 3,3',4,4'-tetrahydroxybiphenyl (BPT) and three isomeric 3,3",4,4"-tetrahydroxyterphenyls (OTT, MTT, PTT) with Alzheimer’s amyloid-β peptide (Aβ) were studied by molecular dynamics simulation and molecular docking. Structural parameters such as Root-mean-square derivations (RMSD), radial distribution function (RDF), helix percentage and other physical parameters were obtained. Th...

Journal: :Marine Drugs 2021

Only palliative therapeutic options exist for the treatment of Alzheimer’s Disease; no new successful drug candidates have been developed in over 15 years. The widely used clinical anticoagulant heparin has reported to exert beneficial effects through multiple pathophysiological pathways involved aetiology Disease, example, amyloid peptide production and clearance, tau phosphorylation, inflamma...

Journal: :Brain : a journal of neurology 2011
Wenlin Hao Yang Liu Shirong Liu Silke Walter Marcus O Grimm Amanda J Kiliaan Botond Penke Tobias Hartmann Claudia E Rübe Michael D Menger Klaus Fassbender

Alzheimer's disease is characterized by extracellular deposits of amyloid β peptide in the brain. Increasing evidence suggests that amyloid β peptide injures neurons both directly and indirectly by triggering neurotoxic innate immune responses. Myeloid differentiation factor 88 is the key signalling molecule downstream to most innate immune receptors crucial in inflammatory activation. For this...

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