Open AccessCerebrospinal Fluid A β 42 Levels: When Physiological Become Pathological State
Author(s) -
Martorana Alessandro,
Di Lorenzo Francesco,
Belli Lorena,
Sancesario Giuseppe,
Toniolo Sofia,
Sallustio Fabrizio,
Sancesario Giulia Maria,
Koch Giacomo
Publication year - 2015
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.12476
Subject(s) - neurodegeneration , neuroscience , pathological , cerebrospinal fluid , disease , medicine , psychology , pathology
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.