Alzheimer’s Disease is the most common form of dementia. 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. The aim of this book is to put all of the recent genetic data on these new genes into context.

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.

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.

The aim of this book is to put all of the recent genetic data on these new genes into contextNew genetics of Alzheimer’s diseaseDifferent genetic variants are discussed, as well as biomarkers and future possibilities ?Includes supplementary material: sn.pub/extras