Evidence map›Paper›PMID 29062035›Full record

ArticleScientific reports2017

CSF tau is associated with impaired cortical plasticity, cognitive decline and astrocyte survival only in APOE4-positive Alzheimer's disease.

Giacomo Koch, Francesco Di Lorenzo, Stefano Loizzo, Caterina Motta, Sara Travaglione, Monica Baiula, Roberto Rimondini, Viviana Ponzo, Sonia Bonnì, Sofia Toniolo and 5 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
3.3field-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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Effect of online tDCS to left somatomotor cortex on neuropsychiatric symptoms among older adults at risk for dementia.Cortex; a journal devoted to the study of the nervous system and behavior · 2023
    Trial
  4. Article
  5. APOE isoform-associated tau oligomer polymorphs differ in synaptotoxicity and seeding activity.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Biomarkers of Activity-Dependent Plasticity and Persistent Enhancement of Synaptic Transmission in Alzheimer Disease: A Review of the Current Status.Medical science monitor : international medical journal of experimental and clinical research · 2023
    Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Network dysfunction in cognitively normal APOE ε4 carriers is related to subclinical tau.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022
    Article
  19. Review
  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

15 authors at 4 institutions in 1 country.

Giacomo KochNon Invasive Brain Stimulation Unit/Department of Behavioral and Clinical Neurology, Santa Lucia Foundation IRCCS, Rome, Italy. g.koch@hsantalucia.it.ORCID 0000-0001-6155-9439
Francesco Di LorenzoNon Invasive Brain Stimulation Unit/Department of Behavioral and Clinical Neurology, Santa Lucia Foundation IRCCS, Rome, Italy.
Stefano LoizzoCenter for Global Health, Italian National Institute of Health, Rome, Italy.
Caterina MottaNon Invasive Brain Stimulation Unit/Department of Behavioral and Clinical Neurology, Santa Lucia Foundation IRCCS, Rome, Italy.
Sara TravaglioneCenter for Global Health, Italian National Institute of Health, Rome, Italy.
Monica BaiulaDepartment of Pharmacy and Biotechnology, University of Bologna, Bologna, Italy.
Roberto RimondiniDepartment of Medical and Surgical Sciences, University of Bologna, Bologna, Italy.
Viviana PonzoNon Invasive Brain Stimulation Unit/Department of Behavioral and Clinical Neurology, Santa Lucia Foundation IRCCS, Rome, Italy.
Sonia BonnìNon Invasive Brain Stimulation Unit/Department of Behavioral and Clinical Neurology, Santa Lucia Foundation IRCCS, Rome, Italy.
Sofia TonioloDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Fabrizio SallustioStroke Unit, Department of Neuroscience, Tor Vergata Policlinic, Rome, Italy.
Marco BozzaliNeuroimaging Laboratory, Santa Lucia Foundation, IRCCS, Rome, Italy.
Carlo CaltagironeNon Invasive Brain Stimulation Unit/Department of Behavioral and Clinical Neurology, Santa Lucia Foundation IRCCS, Rome, Italy.
Gabriele CampanaDepartment of Pharmacy and Biotechnology, University of Bologna, Bologna, Italy.
Alessandro MartoranaNon Invasive Brain Stimulation Unit/Department of Behavioral and Clinical Neurology, Santa Lucia Foundation IRCCS, Rome, Italy.
University of Rome Tor Vergata · ITFondazione Santa Lucia · ITPoliclinico Tor Vergata · ITUniversity of Bologna · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In Alzheimer's disease (AD) patients, apopoliprotein (APOE) polymorphism is the main genetic factor associated with more aggressive clinical course. However, the interaction between cerebrospinal fluid (CSF) tau protein levels and APOE genotype has been scarcely investigated. A possible key mechanism invokes the dysfunction of synaptic plasticity. We investigated how CSF tau interacts with APOE genotype in AD patients. We firstly explored whether CSF tau levels and APOE genotype influence disease progression and long-term potentiation (LTP)-like cortical plasticity as measured by transcranial magnetic stimulation (TMS) in AD patients. Then, we incubated normal human astrocytes (NHAs) with CSF collected from sub-groups of AD patients to determine whether APOE genotype and CSF biomarkers influence astrocytes survival. LTP-like cortical plasticity differed between AD patients with apolipoprotein E4 (APOE4) and apolipoprotein E3 (APOE3) genotype. Higher CSF tau levels were associated with more impaired LTP-like cortical plasticity and faster disease progression in AD patients with APOE4 but not APOE3 genotype. Apoptotic activity was higher when cells were incubated with CSF from AD patients with APOE4 and high tau levels. CSF tau is detrimental on cortical plasticity, disease progression and astrocyte survival only when associated with APOE4 genotype. This is relevant for new therapeutic approaches targeting tau.

Indexed as

Neuronal PlasticityAgedAlzheimer DiseaseApolipoprotein E4ApoptosisAstrocytesCell SurvivalCognitive DysfunctionFemaleGenotypeHumansMaletau ProteinsApolipoprotein E4tau Proteins

Identifiers

PMID29062035
PMCPMC5653826
OpenAlexW2767087329

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.