Synopses & Reviews
The discovery in 1995 that defects in the novel presenilin genes harbor defects which cause up to half of all cases of early onset familial Alzheimer's disease cases has rapidly led to the creation of a new and exciting sub-field in Alzheimer's disease research. This has clearly been evidenced by the fact that over 250 papers have now been published regarding the presenilins since their identification in 1995. One of the earliest findings regarding the role of the presenilins in Alzheimer's disease was the discovery that like familial Alzheimer's disease mutations in the amyloid ß protein precursor gene, those in the presenilins lead to dramatically increased production of ß-amyloid in the brains of AD patients. Additionally, the presenilins appear to play roles in programmed cell death (apoptosis) and in CNS development. The provocative chapters in this book written by some of the most highly respected experts in the area of Alzheimer's disease research present some of the latest information concerning the biological function of the presenilins and how defects in these genes cause Alzheimer's disease. The knowledge contained in this volume should help to accelerate ongoing attempts to develop novel treatments for Alzheimer's disease and related disorders.
Molecular and biochemical studies of Alzheimer's disease have recently undergone a major revolution with the discovery of the presenilin genes. An understanding of the mechanisms by which mutations in the presenilin genes cause neurodegeneration and dementia should greatly facilitate the development of novel strategies for treating Alzheimer's disease and related disorders.
The role of the familial Alzheimer's Disease genes called "presenilins" in causing neuronal cell death and Alzheimer-related pathology.
Table of Contents
Molecluar genetics of the presenilins in Alzheimer's Disease.- Alzheimer's Disease: A matter of dominance.-Metabolism and function of presenilin 1.- Alternative endoproteolysis of the presenilins and familial Alzheimer's disease.-The APP and PS1/2 mutations linked to early onset familial Alzheimer's Disease increase the extracellular concentration of Aß1-42(43).-Mechanistic studies of the effect of presenilins 1 and 2 on APP metabolism.-Presenilin 2 - APP interactions.