Evidence map›Paper›PMID 31066320›Full record

ArticleAutophagy2019

Rapamycin and Alzheimer disease: a double-edged sword?

Julian M Carosi, Timothy J Sargeant

Abstract readComment
In one paragraph

Article in Autophagy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
–field-weighted citation impact
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

64 citing papers in PubMed.

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  12. Microglia, Trem2, and Neurodegeneration.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025
    Review
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4 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Julian M Carosia Hopwood Centre for Neurobiology, Lifelong Health Theme , South Australian Health and Medical Research Institute , Adelaide , South Australia , Australia.
Timothy J Sargeanta Hopwood Centre for Neurobiology, Lifelong Health Theme , South Australian Health and Medical Research Institute , Adelaide , South Australia , Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Numerous studies have reported that inhibition of MTOR (mechanistic target of rapamycin kinase) clearly reduces Alzheimer disease neuropathological hallmarks in mouse models. This has resulted in calls for the use of the MTOR inhibitor rapamycin for the treatment of dementia in humans. Unfortunately, intervention with rapamycin in these mouse studies commenced before or early in the appearance of these pathological hallmarks. Later in Alzheimer disease, when dementia actually manifests, the brain's lysosomal system is severely damaged and treatment with rapamycin is likely to exacerbate this damage. We reassess literature described by a recent perspective article calling for the use of MTOR inhibition in dementia and conclude that rapamycin could be useful, but only in people who are in the earliest stages of Alzheimer disease. We contend that our interpretation of preclinical data concerning use of rapamycin in Alzheimer disease models is necessary if we are to avoid another failed Alzheimer disease drug trial.

Indexed as

Alzheimer DiseaseAutophagyAmyloid beta-PeptidesAnimalsHumansMiceSirolimusTOR Serine-Threonine KinasesAmyloid beta-PeptidesSirolimusTOR Serine-Threonine KinasesAlzheimer diseaseautophagydementialysosomerapamycin

Identifiers

PMID31066320
PMCPMC6613906

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.