Evidence map›Paper›PMID 20944553›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2011

Cognitive and cortical plasticity deficits correlate with altered amyloid-β CSF levels in multiple sclerosis.

Francesco Mori, Silvia Rossi, Giulia Sancesario, Claudia Codecà, Giorgia Mataluni, Fabrizia Monteleone, Fabio Buttari, Hajime Kusayanagi, Maura Castelli, Caterina Motta and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Pooled it
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  7. Review
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  9. Article
  10. In Vivo Molecular Changes in the Retina of Patients With Multiple Sclerosis.Investigative ophthalmology & visual science · 2021
    Article
  11. Review
  12. Article
  13. Amyloid-β PET and CSF in an autopsy-confirmed cohort.Annals of clinical and translational neurology · 2020
    Article
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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

15 authors at 3 institutions in 1 country.

Francesco MoriDipartimento di Neuroscienze, Clinica Neurologica, Università Tor Vergata, Rome, Italy.
Silvia Rossi
Giulia Sancesario
Claudia Codecà
Giorgia Mataluni
Fabrizia Monteleone
Fabio Buttari
Hajime Kusayanagi
Maura Castelli
Caterina Motta
Valeria Studer
Giorgio Bernardi
Giacomo Koch
Sergio Bernardini
Diego Centonze
Fondazione Santa Lucia · ITUniversity of Rome Tor Vergata · ITPoliclinico Tor Vergata · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cognitive dysfunction is of frequent observation in multiple sclerosis (MS). It is associated with gray matter pathology, brain atrophy, and altered connectivity, and recent evidence showed that acute inflammation can exacerbate mental deficits independently of the primary functional system involved. In this study, we measured cerebrospinal fluid (CSF) levels of amyloid-β(1-42) and τ protein in MS and in clinically isolated syndrome patients, as both proteins have been associated with cognitive decline in Alzheimer's disease (AD). In AD, amyloid-β(1-42) accumulates in the brain as insoluble extracellular plaques, possibly explaining why soluble amyloid-β(1-42) is reduced in the CSF of these patients. In our sample of MS patients, amyloid-β(1-42) levels were significantly lower in patients cognitively impaired (CI) and were inversely correlated with the number of Gadolinium-enhancing (Gd+) lesions at the magnetic resonance imaging (MRI). Positive correlations between amyloid-β(1-42) levels and measures of attention and concentration were also found. Furthermore, abnormal neuroplasticity of the cerebral cortex, explored with θ burst stimulation (TBS), was observed in CI patients, and a positive correlation was found between amyloid-β(1-42) CSF contents and the magnitude of long-term potentiation-like effects induced by TBS. No correlation was conversely found between τ protein concentrations and MRI findings, cognitive parameters, and TBS effects in these patients. Together, our results indicate that in MS, central inflammation is able to alter amyloid-β metabolism by reducing its concentration in the CSF and leading to impairment of synaptic plasticity and cognitive function.

Indexed as

Multiple SclerosisAdultAmyloid beta-PeptidesCerebral CortexCognition DisordersEvoked Potentials, MotorFemaleFunctional LateralityGadoliniumHumansLong-Term PotentiationMagnetic Resonance ImagingMaleMiddle AgedMuscle, SkeletalNeuronal PlasticityAmyloid beta-Peptidesamyloid beta-protein (1-42)GadoliniumPeptide Fragmentstau Proteins

Identifiers

PMID20944553
PMCPMC3055691
OpenAlexW1973897310

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.