A surrogate marker for Aβ42 production in the CNS

David M. Holtzman

doi:10.1002/emmm.200900030

Abstract

Alzheimer's disease (AD) is the most common cause of dementia. There are currently no effective treatments that may delay the onset, slow the progression or prevent the disease. Unless such treatments are developed, the number of AD cases is expected to double in the next 30 years. There is overwhelming genetic and biochemical evidence that the aggregation and buildup of the amyloid-β (Aβ) peptide plays a critical role in AD pathogenesis.

Highlights

Alzheimer’s disease (AD) is the most common cause of dementia
Ab is a 38–43 amino acid peptide derived from the transmembrane amyloid precursor protein (APP) (Golde et al, 2000)
It is likely that Early-onset autosomal dominant familial AD (EOAD) is caused by increases in the central nervous system (CNS) production of Ab42 relative to Ab40 (De Strooper, 2007), whether the same applies to late-onset AD (LOAD) remains unanswered

Summary

Introduction

Alzheimer’s disease (AD) is the most common cause of dementia. There are currently no effective treatments that may delay the onset, slow the progression or prevent the disease. Understanding what controls Ab42 levels in the central nervous system (CNS) and how to monitor and assess its production, clearance and aggregation is useful to understand AD pathogenesis as well as for determining risk and monitoring new therapies.

Results

Conclusion