Evidence map›Paper›PMID 41942760›Full record

ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2026

Opposing patterns of blood-brain barrier permeability and Alzheimer's disease biomarkers across APOE genotype.

Francesca Bernocchi, Chiara Giuseppina Bonomi, Martina Poli, Martina Gaia Di Donna, Alessandro Terrinoni, Caterina Motta, Alessandro Martorana

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In one paragraph

Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Rethinking blood-brain barrier permeability in Alzheimer's disease: insights from APOE genotype-specific associations.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
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4 · The record

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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

7 authors.

Francesca BernocchiMemory Clinic and Neurodegenerative Dementia Research Unit, Policlinico Tor Vergata, University of Rome "Tor Vergata", Rome, Italy.
Chiara Giuseppina BonomiMemory Clinic and Neurodegenerative Dementia Research Unit, Policlinico Tor Vergata, University of Rome "Tor Vergata", Rome, Italy.
Martina PoliMemory Clinic and Neurodegenerative Dementia Research Unit, Policlinico Tor Vergata, University of Rome "Tor Vergata", Rome, Italy.
Martina Gaia Di DonnaMemory Clinic and Neurodegenerative Dementia Research Unit, Policlinico Tor Vergata, University of Rome "Tor Vergata", Rome, Italy.
Alessandro TerrinoniDepartment of Experimental Medicine, University of Rome Tor Vergata, Via Montpellier, 1, Rome, 00133, Italy.
Caterina MottaMemory Clinic and Neurodegenerative Dementia Research Unit, Policlinico Tor Vergata, University of Rome "Tor Vergata", Rome, Italy.
Alessandro MartoranaMemory Clinic and Neurodegenerative Dementia Research Unit, Policlinico Tor Vergata, University of Rome "Tor Vergata", Rome, Italy. martorana@med.uniroma2.it.ORCID http://orcid.org/0000-0001-8456-4169

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAPOE is the strongest genetic risk factor for sporadic Alzheimer’s disease (AD), influencing both proteinopathies and cerebrovascular integrity. While the ε4 allele is well studied, the role of ε2—particularly in relation to blood-brain barrier (BBB) permeability—remains underexplored.

objectiveTo investigate the association between APOE genotype, BBB permeability, and AD pathology in a large cohort of biomarker-confirmed AD patients.

methodsWe analyzed data from 895 patients with a CSF-based diagnosis of AD. APOE genotype was determined, and patients were grouped as ε2 (n = 68), ε3 (n = 481), or ε4 carriers (n = 346). CSF Aβ42, p-tau181, t-tau, p-tau181/Aβ42 and QAlb (a marker of BBB permeability) were measured. Group comparisons were conducted using non-parametric tests with Holm-corrected post-hoc analyses.

resultsAPOE ε4 carriers exhibited higher p-tau181/Aβ42, consistent with greater AD pathology. In contrast, APOE ε2 carriers showed higher QAlb values and lower p-tau181/Aβ42, suggesting increased BBB permeability despite lower disease burden.

conclusionOur findings support a potential protective role of APOE ε2 associated with BBB permeability modulation. Further research is warranted to clarify mechanisms linking BBB permeability and disease burden in AD.

Indexed as

Alzheimer DiseaseApolipoproteins EBlood-Brain BarrierAgedAged, 80 and overAmyloid beta-PeptidesApolipoprotein E4BiomarkersFemaleGenotypeHumansMaleMiddle AgedPeptide FragmentsPermeabilitytau ProteinsAmyloid beta-Peptidesamyloid beta-protein (1-42)Apolipoprotein E4Apolipoproteins EBiomarkersPeptide Fragmentstau ProteinsAlzheimer’s diseaseAPOEBlood-brain barrierCerebrospinal fluid biomarkerDisease burden

Identifiers

PMID41942760

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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.