Evidence map›Paper›PMID 26555572›Full record

ReviewCNS neuroscience & therapeutics2015

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

Open access · greenAbstract readReview
In one paragraph

Review in CNS neuroscience & therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. From adolescence to Alzheimer's: a neurodevelopmental lifespan model of cognitive vulnerability.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
  4. Review
  5. Article
  6. Article
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  8. Is blood pTau a reliable indicator of the CSF status? A narrative review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Frontotemporal Dementia, Where Do We Stand? A Narrative Review.International journal of molecular sciences · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Alessandro MartoranaClinica Neurologica, Sytem Medicine Department, University of Rome "Tor Vergata", Rome, Italy.
Francesco Di LorenzoClinica Neurologica, Sytem Medicine Department, University of Rome "Tor Vergata", Rome, Italy.
Lorena BelliClinica Neurologica, Sytem Medicine Department, University of Rome "Tor Vergata", Rome, Italy.
Giuseppe SancesarioClinica Neurologica, Sytem Medicine Department, University of Rome "Tor Vergata", Rome, Italy.
Sofia TonioloClinica Neurologica, Sytem Medicine Department, University of Rome "Tor Vergata", Rome, Italy.
Fabrizio SallustioClinica Neurologica, Sytem Medicine Department, University of Rome "Tor Vergata", Rome, Italy.
Giulia Maria SancesarioDepartment of Clinical and Behavioral Neurology, IRCCS Santa Lucia Foundation, Rome, Italy.
Giacomo KochNon-Invasive Brain Stimulation Unit, Department of Behavioral and Clinical Neurology, Santa Lucia Foundation IRCCS, Rome, Italy.
University of Rome Tor Vergata · ITFondazione Santa Lucia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Amyloid beta-PeptidesAnimalsBiomarkersCognition DisordersHumansPeptide FragmentsSynaptic TransmissionAmyloid beta-Peptidesamyloid beta-protein (1-42)BiomarkersPeptide FragmentsAlzheimer's diseaseAmyloid betaNeural transmissionSynaptopathy

Identifiers

PMID26555572
PMCPMC6493161
OpenAlexW2167785159

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.