Evidence map›Paper›PMID 34406560›Full record

ReviewMetabolic brain disease2022

Neurovascular dysfunction and vascular amyloid accumulation as early events in Alzheimer's disease.

Ricardo Apátiga-Pérez, Luis O Soto-Rojas, B Berenice Campa-Córdoba, Nabil Itzi Luna-Viramontes, Elvis Cuevas, Ignacio Villanueva-Fierro, Miguel Angel Ontiveros-Torres, Marely Bravo-Muñoz, Paola Flores-Rodríguez, Linda Garcés-Ramirez and 4 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Metabolic brain disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

53 citing papers in PubMed, 91 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Brain and retina in Alzheimer's disease: Pathological intersections and estimates from imaging.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  8. Neurometabolic and vascular dysfunction as an early diagnostic for Alzheimer's disease and related dementias.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
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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

14 authors at 6 institutions in 3 countries.

Ricardo Apátiga-PérezNational Dementia BioBank. Ciencias Biológicas. Facultad de Estudios Superiores Cuautitlán, Universidad Nacional 13 Autónoma de México, Estado de México, México.
Luis O Soto-RojasFacultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Estado de México, Mexico.
B Berenice Campa-CórdobaNational Dementia BioBank. Ciencias Biológicas. Facultad de Estudios Superiores Cuautitlán, Universidad Nacional 13 Autónoma de México, Estado de México, México.
Nabil Itzi Luna-ViramontesNational Dementia BioBank. Ciencias Biológicas. Facultad de Estudios Superiores Cuautitlán, Universidad Nacional 13 Autónoma de México, Estado de México, México.
Elvis CuevasDivision of Neurotoxicology, National Center for Toxicological Research/U.S. Food and Drug Administration, Jefferson, AR, USA.
Ignacio Villanueva-FierroCIIDIR, Durango, Instituto Politécnico Nacional, Becario COFAA, Durango, México.
Miguel Angel Ontiveros-TorresTecnologico de Monterrey, Escuela de Ingeniería y Ciencias, Toluca, Estado de México, México.
Marely Bravo-MuñozGrupo Inmensa, Ciencias neurológicas y salud mental, Chiapas, México.
Paola Flores-RodríguezCIIDIR, Durango, Instituto Politécnico Nacional, Becario COFAA, Durango, México.
Linda Garcés-RamirezDepartamento de Fisiología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, México, México.
Fidel de la CruzDepartamento de Fisiología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, México, México.
José Francisco Montiel-SosaNational Dementia BioBank. Ciencias Biológicas. Facultad de Estudios Superiores Cuautitlán, Universidad Nacional 13 Autónoma de México, Estado de México, México.
Mar Pacheco-HerreroNeuroscience Research Laboratory, Faculty of Health Sciences, Pontificia Universidad Católica Madre y Maestra, Santiago de los Caballeros, Dominican Republic. mpacheco@pucmm.edu.do.
José Luna-MuñozNational Dementia BioBank. Ciencias Biológicas. Facultad de Estudios Superiores Cuautitlán, Universidad Nacional 13 Autónoma de México, Estado de México, México. jluna_tau67@comunidad.unam.mx.ORCID 0000-0002-6927-913X
Instituto Politécnico Nacional · MXUniversidad Nacional Autónoma de México · MXNational Center for Toxicological Research · USPontificia Universidad Católica Madre y Maestra · DOTecnológico de Monterrey · MXUniversidad Nacional Pedro Henríquez Ureña · DO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is clinically characterized by a progressive loss of cognitive functions and short-term memory. AD patients present two distinctive neuropathological lesions: neuritic plaques and neurofibrillary tangles (NFTs), constituted of beta-amyloid peptide (Aβ) and phosphorylated and truncated tau proteins. Aβ deposits around cerebral blood vessels (cerebral amyloid angiopathy, CAA) is a major contributor to vascular dysfunction in AD. Vascular amyloid deposits could be early events in AD due to dysfunction in the neurovascular unit (NVU) and the blood-brain barrier (BBB), deterioration of the gliovascular unit, and/or decrease of cerebral blood flow (CBF). These pathological events can lead to decreased Aβ clearance, facilitate a neuroinflammatory environment as well as synaptic dysfunction and, finally, lead to neurodegeneration. Here, we review the histopathological AD hallmarks and discuss the two-hit vascular hypothesis of AD, emphasizing the role of neurovascular dysfunction as an early factor that favors vascular Aβ aggregation and neurodegeneration. Addtionally, we emphasize that pericyte degeneration is a key and early element in AD that can trigger amyloid vascular accumulation and NVU/BBB dysfunction. Further research is required to better understand the early pathophysiological mechanisms associated with NVU alteration and CAA to generate early biomarkers and timely treatments for AD.

Indexed as

Alzheimer DiseaseCerebral Amyloid AngiopathyAmyloid beta-PeptidesBrainHumansPlaque, AmyloidAmyloid beta-PeptidesAlzheimer´s diseaseCerebral amyloid angiopathyNeuroinflammationNeurovascular dysfunctionPericyte degeneration

Identifiers

PMID34406560
OpenAlexW3194869754

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.