Cerebrospinal Fluid Aβ42 Levels: When Physiological Become Pathological State. (11th November 2015)

• Record Type: Journal Article
• Authors: Martorana, Alessandro; Di Lorenzo, Francesco; Belli, Lorena; Sancesario, Giuseppe; Toniolo, Sofia; Sallustio, Fabrizio; Sancesario, Giulia Maria; Koch, Giacomo
• Is Part Of: CNS neuroscience & therapeutics. Volume 21:Number 12(2015)
• Page Start: 921
• Page End: 925
• Publication Date: 2015-11-11
• Subjects: Alzheimer's disease -- Amyloid beta -- Neural transmission -- Synaptopathy; Neuropharmacology -- Periodicals; Central nervous system -- Diseases -- Effect of drugs on -- Periodicals; 612.8
• DOI: 10.1111/cns.12476
• Languages: English
• ISSNs: 1755-5930

Abstract

Summary: Impaired amyloid beta (A β ) metabolism is currently considered central to understand the pathophysiology of Alzheimer's disease (AD). Measurements of cerebrospinal fluid A β levels remain the most useful marker for diagnostic purposes and to individuate people at risk for AD. Despite recent advances criticized the direct role in neurodegeneration of cortical neurons, A β is considered responsible for synaptopathy and impairment of neurotransmission and therefore remains the major trigger of AD and future pharmacological treatment remain A β oriented. However, experimental and clinical findings showed that A β peptides could have a wider range of action responsible for cell dysfunction and for appearance of clinico‐pathological entities different from AD. Such findings may induce misunderstanding of the real role played by A β in AD and therefore strengthen criticism on its centrality and need for CSF measurements. Aim of this review is to discuss the role of CSF A β levels in light of experimental, clinical pathologic, and electrophysiological results in AD and other pathological entities to put in a correct frame the value of A β changes.