Evidence map›Paper›PMID 26715389›Full record

ReviewCNS drugs2016

The Benzodiazepine-Dementia Disorders Link: Current State of Knowledge.

Antoine Pariente, Sophie Billioti de Gage, Nicholas Moore, Bernard Bégaud

Abstract readReview
PubMed Publisher
In one paragraph

Review in CNS drugs, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 4 pooled it
8.6field-weighted citation impact, top 1% 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

48 citing papers in PubMed, 4 syntheses or guidelines pooled it, 124 citations in OpenAlex.

  1. Pooled it
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  12. Symptomatic and neurotrophic effects of GABAA receptor positive allosteric modulation in a mouse model of chronic stress.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022
    Article
  13. Review
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  20. Benzodiazepine use and the risk of dementia.Alzheimer's & dementia (New York, N. Y.) · 2022
    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 2 institutions in 1 country.

Antoine ParienteINSERM, U657-Pharmacoepidemiology, Université de Bordeaux, 146 rue Léo Saignat, 33076, Bordeaux cedex, France. antoine.pariente@u-bordeaux.fr.
Sophie Billioti de GageINSERM, U657-Pharmacoepidemiology, Université de Bordeaux, 146 rue Léo Saignat, 33076, Bordeaux cedex, France.
Nicholas MooreINSERM, U657-Pharmacoepidemiology, Université de Bordeaux, 146 rue Léo Saignat, 33076, Bordeaux cedex, France.
Bernard BégaudINSERM, U657-Pharmacoepidemiology, Université de Bordeaux, 146 rue Léo Saignat, 33076, Bordeaux cedex, France.
Inserm · FRUniversité de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The short-term effects of benzodiazepines on memory are well established and are suspected in the long term. Eleven studies have been published so far concerning benzodiazepine use and the risk of dementia disorders; nine of these studies concluded these drugs have a deleterious effect, one found a protective effect, and one (the most recently published) observed no effect. The positive association found in some studies could be due to a reverse causation bias since the main indications for benzodiazepines (e.g. sleep disorders, anxiety) can also be prodromes of dementia disorders. This bias is less likely for treatments started more than 10 years before the diagnosis. Among others, three mechanisms could underlie the potential influence of benzodiazepines on the development of dementia disorders. First, benzodiazepines can decrease beta-site amyloid precursor protein-cleaving enzyme 1 (BACE-1) and γ-secretase activity and slow down the accumulation of Aβ oligomers in the brain. This potential positive effect has never been confirmed; the same is true for the prevention of excitotoxicity through benzodiazepine anti-glutamatergic action. Second, since astrocytes located in the area of amyloid plaques could have gamma-aminobutyric acid (GABA)-secreting activity, patients with pre-dementia lesions could be at increased risk of presenting with more pronounced deleterious cognitive effects of benzodiazepines. Finally, owing to the neural compensation and cognitive reserve concepts, some subjects could cope with initial lesions by using/developing alternative networks. By lowering the brain activation level, benzodiazepines could limit this capacity. In conclusion, it is essential that animal studies explore the mechanistic hypotheses of this association found by most of the pharmacoepidemiological studies conducted on this topic.

Indexed as

Anxiety DisordersBenzodiazepinesBiasDementiaDepressionHumansRiskSleep Wake DisordersBenzodiazepines

Identifiers

PMID26715389
OpenAlexW2203369238

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.