Evidence map›Paper›PMID 42444286›Full record

ArticleEuropean journal of neurology2026

Vascular-Apoptotic Crosstalk in Alzheimer's Disease: The Possible Role of Vascular Senescence in Blood-Brain Barrier Dysfunction.

Carlangelo Carrese, Chiara Giuseppina Bonomi, Francesca Bernocchi, Martina Gaia Di Donna, Martina Poli, Guido Greco, Nicola Biagio Mercuri, Alessandro Martorana, Caterina Motta

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in European journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Carlangelo CarreseMemory Clinic and Neurodegenerative Dementia Research Unit, University of Rome "Tor Vergata", Rome, Italy.
Chiara Giuseppina BonomiMemory Clinic and Neurodegenerative Dementia Research Unit, University of Rome "Tor Vergata", Rome, Italy.
Francesca BernocchiMemory Clinic and Neurodegenerative Dementia Research Unit, University of Rome "Tor Vergata", Rome, Italy.
Martina Gaia Di DonnaMemory Clinic and Neurodegenerative Dementia Research Unit, University of Rome "Tor Vergata", Rome, Italy.ORCID https://orcid.org/0000-0001-8320-2887
Martina PoliMemory Clinic and Neurodegenerative Dementia Research Unit, University of Rome "Tor Vergata", Rome, Italy.ORCID https://orcid.org/0009-0000-4882-9895
Guido GrecoMemory Clinic and Neurodegenerative Dementia Research Unit, University of Rome "Tor Vergata", Rome, Italy.
Nicola Biagio MercuriNeurology Unit, Policlinico Tor Vergata, University of Rome "Tor Vergata", Rome, Italy.
Alessandro MartoranaMemory Clinic and Neurodegenerative Dementia Research Unit, University of Rome "Tor Vergata", Rome, Italy.ORCID https://orcid.org/0000-0001-8456-4169
Caterina MottaMemory Clinic and Neurodegenerative Dementia Research Unit, University of Rome "Tor Vergata", Rome, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBlood-brain barrier (BBB) dysfunction is an early feature of Alzheimer's disease (AD), influenced by amyloid pathology, astrocyte activation, and vasoactive mediators such as endothelin-1 (ET-1). ET-1 has been implicated in apoptosis and vascular senescence through induction of p53, a pro-apoptotic factor, whereas BCL-X exerts antiapoptotic effects. We investigated the interplay between ET-1, p53, and BCL-X in AD and their contribution to BBB permeability.

methodsWe studied 101 individuals (70 AD, 31 controls) who underwent cerebrospinal fluid (CSF) analysis for Aβ42, p-tau, ET-1, p53, BCL-X, and the CSF/serum albumin quotient (QAlb), an index of BBB permeability. Correlations between biomarkers were explored, followed by multiple regression and mediation analysis to assess whether p53 mediated the ET-1-BBB relationship.

resultsNo absolute differences in ET-1, p53, or BCL-X were found between AD and controls. However, in AD, ET-1 correlated positively with p53 and negatively with BCL-X, whereas no such associations were seen in controls. None of these biomarkers related to the p-tau/Aβ42 ratio. Regression analysis identified both ET-1 and p53 as independent predictors of BBB permeability. Mediation analysis further revealed that ET-1 influenced BBB permeability both directly and indirectly through p53.

conclusionOur findings suggest that AD is characterized less by absolute biomarker changes and more by altered interrelationships linking ET-1, apoptosis, and BBB integrity. ET-1 may promote BBB dysfunction partly via p53, which is consistent with the mechanisms of vascular senescence. These results highlight apoptosis-vascular interactions as potential drivers of BBB impairment in AD.

Indexed as

Alzheimer DiseaseApoptosisBlood-Brain BarrierEndothelin-1Tumor Suppressor Protein p53AgedAged, 80 and overAmyloid beta-Peptidesbcl-X ProteinBiomarkersFemaleHumansMalePeptide Fragmentstau ProteinsAmyloid beta-Peptidesbcl-X ProteinBiomarkersEndothelin-1Peptide Fragmentstau ProteinsTumor Suppressor Protein p53Alzheimers diseaseapoptosisblood–brain barrierendothelin‐1senescence

Identifiers

PMID42444286
PMCPMC13365876

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.