New Thinking on the Etiology and Pathogenesis of Late-Onset Alzheimer's Disease

Alan P Hudson,Keith Crutcher,Stephen Robinson,Brian J Balin

doi:10.4061/2011/848395

Abstract

New Thinking on the Etiology and Pathogenesis of Late-Onset Alzheimer's Disease

Highlights

Substantial evidence derived from clinical trials, animal model studies, and other sources indicates that late-onset Alzheimer’s disease (AD) cannot be explained solely or primarily by accumulating NSP and NFT despite the fact that these are the most obvious and consistent pathological features of this disease
The first paper included in this special issue presents an interesting, and we think cogent, argument for a reconsideration of the amyloid cascade hypothesis
Since firm diagnosis of late-onset AD depends on postmortem examination of the brain of affected individuals, a pressing need exists for identification of markers that can reliably indicate the presence of AD in individuals at much earlier stages of the disease induction process

Summary

Introduction

The first paper included in this special issue presents an interesting, and we think cogent, argument for a reconsideration of the amyloid cascade hypothesis. Substantial evidence derived from clinical trials, animal model studies, and other sources indicates that late-onset AD cannot be explained solely or primarily by accumulating NSP and NFT despite the fact that these are the most obvious and consistent pathological features of this disease.

Results

Conclusion