Genetic Variants in Alzheimer's Disease

ISBN-13: 9781489997999 / Angielski / Miękka / 2015 / 254 str.

Minerva M. Carrasquillo; Kevin Morgan

Opis

Alzheimer's Disease is the most common form of dementia. The disease is characterised by the loss of synapses and neurons in the cerebral cortex and certain subcortical regions. In the last three years, the genetics of Alzheimer's Disease has made significant advances; in fact, one could argue more than in the previous two decades. This has resulted in the identification of nine new genes and perhaps more importantly the realization that new pathways could be involved in the pathogenesis of Alzheimer's. These new pathways are now legitimate targets for therapeutic intervention, which can possibly lead to treatment or a possible cure. The aim of this book is to put all of the recent genetic data on these new genes into context. Different genetic variants will be discussed, as well as biomarkers and future possibilities. ​

Spis treści

The Genetics of Alzheimer’s disease: Introduction and Perspective for the Future.- Apolipoprotein E .- Clusterin.- PICALM.- Complement Component (3b/4b) Receptor 1(CR1).- Bridging Integrator 1 (BIN1).- ATP-binding cassette, sub-family A (ABC1), member 7 (ABCA7).- Membrane-spanning 4-domains subfamily A, MS4A cluster.- Sialic acid binding immunoglobulin-like lectin-3 (CD33).- Erythropoietin-producing human hepatocellular carcinoma (EphA1).- CD2-associated protein (CD2AP).- Other Genes Implicated in Alzheimer’s Disease.- The Future Role of Biomarkers in Alzheimer’s Disease Diagnostics.- Index.

Blurb

Since 2009, a revolution has been witnessed in Alzheimer’s Disease genetics. New genetic links are being discovered at an unprecedented pace and our understanding of the molecular mechanisms of neurodegeneration have taken a quantum leap forward. This book provides a thorough description of the genes that have been implicated in the aetiology of late-onset Alzheimer’s disease (LOAD) based on evidence of genetic association. These “AD susceptibility genes” are described both in their genomic and cellular context, as well as with respect to their known or suspected molecular functions. Although these genes are not sufficient to explain all of the genetic contributions to LOAD, they represent the best replicated set of genes to date. Undoubtedly the list will grow as more advanced genomic approaches towards the identification of novel LOAD genes progresses.