Evidence map›Paper›PMID 34867298›Full record

ReviewFrontiers in aging neuroscience2021

Carbonic Anhydrases as Potential Targets Against Neurovascular Unit Dysfunction in Alzheimer's Disease and Stroke.

Nicole Lemon, Elisa Canepa, Marc A Ilies, Silvia Fossati

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in aging neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Acidosis, Iron Dyshomeostasis and Inflammatory Injury.International journal of molecular sciences · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Introduction to Carbonic Anhydrase.Sub-cellular biochemistry · 2026
    Review
  10. Article
  11. Article
  12. Article
  13. Cerebral proteome adaptations to amyloid angiopathy are prevented by carbonic anhydrase inhibitors.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  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

4 authors at 1 institution in 1 country.

Nicole LemonAlzheimer's Center at Temple (ACT), Lewis Katz School of Medicine, Temple University, Philadelphia, PA, United States.
Elisa CanepaAlzheimer's Center at Temple (ACT), Lewis Katz School of Medicine, Temple University, Philadelphia, PA, United States.
Marc A IliesAlzheimer's Center at Temple (ACT), Lewis Katz School of Medicine, Temple University, Philadelphia, PA, United States.
Silvia FossatiAlzheimer's Center at Temple (ACT), Lewis Katz School of Medicine, Temple University, Philadelphia, PA, United States.
Temple University · US

Funding

Potentiation of CAA-mediated endothelial dysfunction by cardiovascular risk factorsR01NS104127 · NINDS · TEMPLE UNIV OF THE COMMONWEALTH · PI FOSSATI, SILVIA · 2018 to 2022
$3.0M
Targeting carbonic anhydrases in Alzheimer's diseaseR01AG062572 · NIA · TEMPLE UNIV OF THE COMMONWEALTH · PI FOSSATI, SILVIA · 2019 to 2023
$2.3M
NIA NIH HHS R01 AG062572NINDS NIH HHS R01 NS104127
6 · The paper itself

Abstract

The Neurovascular Unit (NVU) is an important multicellular structure of the central nervous system (CNS), which participates in the regulation of cerebral blood flow (CBF), delivery of oxygen and nutrients, immunological surveillance, clearance, barrier functions, and CNS homeostasis. Stroke and Alzheimer Disease (AD) are two pathologies with extensive NVU dysfunction. The cell types of the NVU change in both structure and function following an ischemic insult and during the development of AD pathology. Stroke and AD share common risk factors such as cardiovascular disease, and also share similarities at a molecular level. In both diseases, disruption of metabolic support, mitochondrial dysfunction, increase in oxidative stress, release of inflammatory signaling molecules, and blood brain barrier disruption result in NVU dysfunction, leading to cell death and neurodegeneration. Improved therapeutic strategies for both AD and stroke are needed. Carbonic anhydrases (CAs) are well-known targets for other diseases and are being recently investigated for their function in the development of cerebrovascular pathology. CAs catalyze the hydration of CO

Indexed as

Alzheimer’s diseaseamyloid betacarbonic anhydrase (CA)cerebrovascular pathologyinflammationmitochondrianeurovascular unit (NVU)stroke

Identifiers

PMID34867298
PMCPMC8635164
OpenAlexW3211943424

What Socratic 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 Socratic graph.