Evidence map›Paper›PMID 26993506›Full record

ReviewCellular and molecular neurobiology2016

Neurovascular and Cognitive failure in Alzheimer's Disease: Benefits of Cardiovascular Therapy.

Edith Hamel, Jessika Royea, Brice Ongali, Xin-Kang Tong

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cellular and molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 7% 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, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

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  16. Role of cortical microbleeds in cognitive impairment: In vivo behavioral and imaging characterization of a novel murine model.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
    Article
  17. Article
  18. Within the Brain: The Renin Angiotensin System.International journal of molecular sciences · 2018
    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

4 authors at 1 institution in 1 country.

Edith HamelLaboratory of Cerebrovascular Research, Montreal Neurological Institute, McGill University, 3801 University Street, Suite 748, Montréal, QC, H3A 2B4, Canada. edith.hamel@mcgill.ca.
Jessika RoyeaLaboratory of Cerebrovascular Research, Montreal Neurological Institute, McGill University, 3801 University Street, Suite 748, Montréal, QC, H3A 2B4, Canada.
Brice OngaliLaboratory of Cerebrovascular Research, Montreal Neurological Institute, McGill University, 3801 University Street, Suite 748, Montréal, QC, H3A 2B4, Canada.
Xin-Kang TongLaboratory of Cerebrovascular Research, Montreal Neurological Institute, McGill University, 3801 University Street, Suite 748, Montréal, QC, H3A 2B4, Canada.
Montreal Neurological Institute and Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a multifactorial and multifaceted disease for which we currently have very little to offer since there is no curative therapy, with only limited disease-modifying drugs. Recent studies in AD mouse models that recapitulate the amyloid-β (Aβ) pathology converge to demonstrate that it is possible to salvage cerebrovascular function with a variety of drugs and, particularly, therapies used to treat cardiovascular diseases such as hypercholesterolemia and hypertension. These drugs can reestablish dilatory function mediated by various endothelial and smooth muscle ion channels as well as nitric oxide availability, benefits that result in normalized brain perfusion. These cerebrovascular benefits would favor brain perfusion, which may help maintain neuronal function and, possibly, delay cognitive failure. However, restoring cerebrovascular function in AD mouse models was not necessarily accompanied by rescue of cognitive deficits related to spatial learning and memory. The results with cardiovascular therapies rather suggest that drugs originally designed to treat cardiovascular diseases that concurrently restore cerebrovascular and cognitive function do so through their pleiotropic effects. Specifically, recent findings suggest that these drugs act directly on brain cells and neuronal pathways involved in memory formation, hence, working simultaneously albeit independently on neuronal and vascular targets. These findings may help select medications for patients with cardiovascular diseases at risk of developing AD with increasing age. Further, they may identify molecular targets for recovering memory pathways that bear potential for new therapeutic avenues.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainCognition DisordersHumansLosartanSimvastatinAmyloid beta-PeptidesLosartanSimvastatinAngiotensin receptor blockerCardiovascular therapyCerebrovascular reactivityMemory pathwaysStatinVascular oxidative stress

Identifiers

PMID26993506
PMCPMC11482419
OpenAlexW2302900085

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.