Research Progress in Alzheimer's Disease and Dementia, Том 3Nova Publishers, 2007 - Всего страниц: 438 Alzheimer's disease (AD), the most common form of neurodegenerative disorder in the elderly, is characterised pathologically by extracellular amyloid plaques and intracellular neurofibrillary tangles, pathophysiologically by synaptic dysfunction, and clinically by a progressive decline in cognition. Currently, AD has no cure and its prevalence is predicted to triple by 2050 with the rapid increase in the ageing population, unless more effective treatments are developed. Since the publication of the second book volume, the rapid progress in the research fields of AD and dementia continues through the intensive efforts of research scientists worldwide. This third book volume contains 15 chapters, bringing together a presentation of research frontiers in current AD/dementia research. The topics include molecular genetics of AD, gene expression abnormalities in AD progression, presenilins, taupathy in AD, single -induced(neuron gene expression abnormalities in AD, intracellular A neurodegeneration, roles of lipoprotein receptors in AD onset and progression, cholesterol and tau hyperphosphorylation, AD diagnostics and therapeutic strategies, in vivo visualisation of amyloid-like structures, cathepsin B, antiamyloidogenesis and neuroprotection, environmental enrichment, Fragile X mental retardation gene and dementia, category learning in Parkinson's disease, cerebrovascular disease and dementia, and dementia and hypertension. These chapters cover current advances in our understanding of the pathogenic mechanisms underlying AD and dementia, in the diagnosis of early AD and dementia, and in the development of therapeutic agents that target memory-relevant AD pathogenesis. The book will be highly valuable to students and scientists worldwide who are interested in the scientific research progress in AD and dementia. |
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... neprilysin , an Aẞ degrading enzyme , is regulated by y - secretase activity . In vitro studies show that transcription from neprilysin gene promoter can be activated by cytosolic domains released from APP , APLP1 or APLP2 by y ...
... neprilysin , an Aẞ degrading enzyme , is regulated by y - secretase activity . In vitro studies show that transcription from neprilysin gene promoter can be activated by cytosolic domains released from APP , APLP1 or APLP2 by y ...
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... neprilysin by intracellular domains of betaAPP and APLP . Neuron 46 : 541-554 , 2005 . Parent , A.T. , N.Y. Barnes , Y. Taniguchi , G. Thinakaran and S.S. Sisodia . Presenilin attenuates receptor - mediated signaling and synaptic ...
... neprilysin by intracellular domains of betaAPP and APLP . Neuron 46 : 541-554 , 2005 . Parent , A.T. , N.Y. Barnes , Y. Taniguchi , G. Thinakaran and S.S. Sisodia . Presenilin attenuates receptor - mediated signaling and synaptic ...
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Research Progress in Alzheimer's Disease and Dementia, Том 3 Miao-Kun Sun Ограниченный просмотр - 2007 |
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Abeta Acad activity aggregates allele Alzheimer disease Alzheimer's disease amyloid deposition amyloid plaques amyloid precursor protein antibody APOE apolipoprotein Aẞ oligomers Aẞ peptides associated binding Biol blood pressure Braak CatB category learning cell cellular cerebral Chem cholesterol chromosome cleavage clinical cognitive decline correlates cortex cortical deficits dementia domain endosomes enrichment entorhinal cortex enzyme fibrils function gene expression Genet Ginsberg hippocampus human hyperphosphorylated imaging increased inhibition inhibitors interaction intracellular intraneuronal Aẞ lipoprotein receptors LRP1 membrane memory metabolism microtubule mild cognitive impairment molecular mouse model mRNA mutations Natl neprilysin Neurobiol Neurochem neurodegenerative neurofibrillary tangles Neurology neuronal loss neurons neuropathology Neurosci NFTs nicastrin Oddo oligomeric oligomers Parkinson's disease pathogenesis pathology pathway PD patients peptide phosphorylation presenilin Proc processing regulation risk factor role Selkoe soluble sorLA ẞ-amyloid studies synaptic syndrome tau protein trafficking transgenic transgenic mice vascular vascular dementia vitro vivo Wang y-secretase