Journal Article10.1016/J.NBD.2007.04.004
Ageing and amyloid-beta peptide deposition contribute to an impaired brain tissue plasminogen activator activity by different mechanisms.
Mathias Cacquevel,Séverine Launay,Hervé Castel,Karim Benchenane,Simon Chéenne,Luc Buée,Lieve Moons,André Delacourte,Peter Carmeliet,Denis Vivien +9 more
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TL;DR: Data support a model in which amyloid deposition induces a decrease in tPA activity through the overproduction of PAI-1 by activated glial cells, and this effect was worsened in mice overproducing Abeta peptides.
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About: This article is published in Neurobiology of Disease. The article was published on 01 Aug 2007. The article focuses on the topics: Plasminogen activator & Tissue plasminogen activator.
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Abeta-degrading enzymes in Alzheimer's disease.
TL;DR: Reductions in neprilysin, IDE and plasmin in AD have been associated with possession of APOEepsilon4, and the level and activity of ACE are increased, the level being directly related to Abeta plaque load.
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Multiplexed Immunoassay Panel Identifies Novel CSF Biomarkers for Alzheimer's Disease Diagnosis and Prognosis
Rebecca Craig-Schapiro,Max Kuhn,Chengjie Xiong,Eve H. Pickering,Jingxia Liu,Thomas P. Misko,Richard J. Perrin,Kelly R. Bales,Holly Soares,Anne M. Fagan,David M. Holtzman +10 more
TL;DR: A targeted proteomics approach to discover novel cerebrospinal fluid (CSF) biomarkers that can augment the diagnostic and prognostic accuracy of current leading CSF biomarkers (Aβ42, tau, p-tau181) and identify a novel biomarker (calbindin) with significant prognostic potential.
Molecular and cellular aspects of protein misfolding and disease
TL;DR: This review summarizes the structural composition of proteins and the current knowledge of underlying forces that lead proteins to lose their native structure and describes the molecular and cellular mechanisms that are associated with protein misfolding in disease.
229
Aging, Cellular Senescence, and Alzheimer’s Disease
TL;DR: It is believed that the removal of senescent cells represents a promising approach toward the effective treatment of aging-related diseases, such as AD, and a review summarizes recent advances.
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Guy M. McKhann,David A. Drachman,Marshall F. Folstein,Robert Katzman,Donald L. Price,Emanuel M. Stadlan +5 more
TL;DR: The criteria proposed are intended to serve as a guide for the diagnosis of probable, possible, and definite Alzheimer's disease; these criteria will be revised as more definitive information becomes available.
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The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics
John Hardy,Dennis J. Selkoe +1 more
TL;DR: It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid β-peptide in plaques in brain tissue and the rest of the disease process is proposed to result from an imbalance between Aβ production and Aβ clearance.
Editorial on Consensus Recommendations for the Postmortem Diagnosis of Alzheimer Disease from the National Institute on Aging and the Reagan Institute Working Group on Diagnostic Criteria for the Neuropathological Assessment of Alzheimer Disease
TL;DR: The consensus recommendations for improving the neuropathological criteria for the postmortem diagnosis of Alzheimer's disease are reported here, and the "position papers" by members of the Working Group that accompany this report elaborate on the research findings and concepts upon which these recommendations were based.
The serpins are an expanding superfamily of structurally similar but functionally diverse proteins - Evolution, mechanism of inhibition, novel functions, and a revised nomenclature
Gary A. Silverman,Phillip I. Bird,Robin W. Carrell,Frank C. Church,Paul Bernard Coughlin,Peter G.W. Gettins,James A. Irving,David A. Lomas,Cliff J. Luke,Richard W. Moyer,Philip A. Pemberton,Eileen Remold-O'Donnell,Guy S. Salvesen,James Travis,James C. Whisstock +14 more
TL;DR: This work aims to provide a systematic literature review and meta-analyses of the determinants of blood clotting disorders and their Kessler’s disease progression as well as some of the mechanisms behind these reactions.
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Deciphering the molecular basis of memory failure in Alzheimer's disease.
TL;DR: Experiments in rodents suggest that soluble oligomers of the amyloid beta protein (Abeta) may discretely interfere with synaptic mechanisms mediating aspects of learning and memory, including long-term potentiation.
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