title: Cerebrospinal Fluid Aβ42 Levels: When Physiological Become Pathological State.
abstract: Impaired amyloid beta (Aβ) metabolism is currently considered central to understand the pathophysiology of Alzheimer's disease (AD). Measurements of cerebrospinal fluid Aβ 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, Aβ is considered responsible for synaptopathy and impairment of neurotransmission and therefore remains the major trigger of AD and future pharmacological treatment remain Aβ oriented. However, experimental and clinical findings showed that Aβ 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 Aβ 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 Aβ 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 Aβ changes.
authors.affiliation: Clinica Neurologica, Sytem Medicine Department, University of Rome "Tor Vergata", Rome, Italy.
authors.forename: Alessandro
authors.initials: A
authors.lastname: Martorana
authors.affiliation: Clinica Neurologica, Sytem Medicine Department, University of Rome "Tor Vergata", Rome, Italy.|Non-Invasive Brain Stimulation Unit, Department of Behavioral and Clinical Neurology, Santa Lucia Foundation IRCCS, Rome, Italy.
authors.forename: Francesco
authors.initials: F
authors.lastname: Di Lorenzo
authors.affiliation: Clinica Neurologica, Sytem Medicine Department, University of Rome "Tor Vergata", Rome, Italy.
authors.forename: Lorena
authors.initials: L
authors.lastname: Belli
authors.affiliation: Clinica Neurologica, Sytem Medicine Department, University of Rome "Tor Vergata", Rome, Italy.
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Sancesario
authors.affiliation: Clinica Neurologica, Sytem Medicine Department, University of Rome "Tor Vergata", Rome, Italy.
authors.forename: Sofia
authors.initials: S
authors.lastname: Toniolo
authors.affiliation: Clinica Neurologica, Sytem Medicine Department, University of Rome "Tor Vergata", Rome, Italy.
authors.forename: Fabrizio
authors.initials: F
authors.lastname: Sallustio
authors.affiliation: Department of Clinical and Behavioral Neurology, IRCCS Santa Lucia Foundation, Rome, Italy.
authors.forename: Giulia Maria
authors.initials: GM
authors.lastname: Sancesario
authors.affiliation: Non-Invasive Brain Stimulation Unit, Department of Behavioral and Clinical Neurology, Santa Lucia Foundation IRCCS, Rome, Italy.
authors.forename: Giacomo
authors.initials: G
authors.lastname: Koch
mesh_terms: D016229:Amyloid beta-Peptides / Q000134:cerebrospinal fluid*; D000818:Animals; D015415:Biomarkers / Q000134:cerebrospinal fluid; D003072:Cognition Disorders / Q000134:cerebrospinal fluid; D006801:Humans; D010446:Peptide Fragments / Q000134:cerebrospinal fluid*; D009435:Synaptic Transmission / Q000502:physiology
chemical_list: D016229:Amyloid beta-Peptides; D015415:Biomarkers; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42)
keywords: Alzheimer's disease; Amyloid beta; Neural transmission; Synaptopathy