Evidence map›Paper›PMID 29320772›Full record

ReviewGerontology2018

A Perfect sTORm: The Role of the Mammalian Target of Rapamycin (mTOR) in Cerebrovascular Dysfunction of Alzheimer's Disease: A Mini-Review.

Candice E Van Skike, Veronica Galvan

Open access · bronzeAbstract readReview
In one paragraph

Review in Gerontology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
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  6. Article
  7. Review
  8. Review
  9. Article
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  11. Article
  12. Neuroprotective Effect of SGLT2 Inhibitors.Molecules (Basel, Switzerland) · 2021
    Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. mTOR Attenuation with Rapamycin Reverses Neurovascular Uncoupling and Memory Deficits in Mice Modeling Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  18. Review
  19. Article
  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

2 authors at 1 institution in 1 country.

Candice E Van SkikeDepartment of Cellular and Integrative Physiology and The Barshop Institute for Longevity and Aging Studies, University of Texas Health San Antonio, San Antonio, TX, USA.
Veronica Galvan
The University of Texas Health Science Center at San Antonio · US

Funding

TRANSGENIC COREP30AG013319 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI JAMES FLOYD NELSON · 1995 to 2026
$30.6M
TRAINING GRANT ON THE BIOLOGY OF AGINGT32AG021890 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Erzsebet Kokovay, JAMES FLOYD NELSON · 2003 to 2026
$11.4M
Brain cellular senescence as a driver of Alzheimers DiseaseRF1AG057964 · NIA · OREGON STATE UNIVERSITY · PI GALVAN, VERONICA, MAGNUSSON, KATHY R · 2017 to 2019
$2.3M
Proteomic analysis of Amyloid Precursor Protein signaling: mediators of toxicityR21AG031380 · NIA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KOURAKINE, ALEXEI · 2008 to 2009
$410k
Pathogenic Tau Promotes Brain Vascular Dysfunction in Alzheimer's DiseaseI01BX002211 · VA · SOUTH TEXAS VETERANS HEALTH CARE SYSTEM · PI GALVAN, VERONICA · 2015 to 2025
–
BLRD VA I01 BX002211NIA NIH HHS P30 AG013319NIA NIH HHS R21 AG031380NIA NIH HHS RF1 AG057964NIA NIH HHS T32 AG021890
6 · The paper itself

Abstract

Cerebrovascular dysfunction is detected prior to the onset of cognitive and histopathological changes in Alzheimer's disease (AD). Increasing evidence indicates a critical role of cerebrovascular dysfunction in the initiation and progression of AD. Recent studies identified the mechanistic/mammalian target of rapamycin (mTOR) as a critical effector of cerebrovascular dysfunction in AD. mTOR has a key role in the regulation of metabolism, but some mTOR-dependent mechanisms are uniquely specific to the regulation of cerebrovascular function. These include the regulation of cerebral blood flow, blood-brain barrier integrity and maintenance, neurovascular coupling, and cerebrovascular reactivity. This article examines the available evidence for a role of mTOR-driven cerebrovascular dysfunction in the pathogenesis of AD and of vascular cognitive impairment and dementia (VCID) and highlights the therapeutic potential of targeting mTOR and/or specific downstream effectors for vasculoprotection in AD, VCID, and other age-associated neurological diseases with cerebrovascular etiology.

Indexed as

Alzheimer DiseaseBlood-Brain BarrierCerebrovascular CirculationCerebrovascular DisordersCognitive DysfunctionDementiaDementia, VascularHumansTOR Serine-Threonine KinasesMTOR protein, humanTOR Serine-Threonine KinasesAlzheimer’s diseaseBlood-brain barrierCerebral blood flowmTORNeurovascular couplingRapamycinVascular density

Identifiers

PMID29320772
PMCPMC5876078
OpenAlexW2784231292

What Socratic holds

Textmetadata
LicenceTDM
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.