Cerebrospinal Fluid Aβ42 Levels: When Physiological Become Pathological State

Alessandro Martorana, Francesco Di Lorenzo, Lorena Belli, Giuseppe Sancesario, Sofia Toniolo, Fabrizio Sallustio, Giulia Maria Sancesario, Giacomo Koch

Research output: Contribution to journalArticle

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.

Original languageEnglish
Pages (from-to)921-925
Number of pages5
JournalCNS Neuroscience and Therapeutics
Volume21
Issue number12
DOIs
Publication statusPublished - Dec 1 2015

Keywords

  • Alzheimer's disease
  • Amyloid beta
  • Neural transmission
  • Synaptopathy

ASJC Scopus subject areas

  • Pharmacology (medical)
  • Physiology (medical)
  • Psychiatry and Mental health
  • Pharmacology

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  • Cite this

    Martorana, A., Di Lorenzo, F., Belli, L., Sancesario, G., Toniolo, S., Sallustio, F., Sancesario, G. M., & Koch, G. (2015). Cerebrospinal Fluid Aβ42 Levels: When Physiological Become Pathological State. CNS Neuroscience and Therapeutics, 21(12), 921-925. https://doi.org/10.1111/cns.12476