Evidence map›Paper›PMID 28294066›Full record

ReviewCurrent neuropharmacology2017

Mechanisms of Melatonin in Alleviating Alzheimer's Disease.

Mayuri Shukla, Piyarat Govitrapong, Parichart Boontem, Russel J Reiter, Jutamaad Satayavivad

Open access · bronzeAbstract readReview
In one paragraph

Review in Current neuropharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 1 pooled it
7.3field-weighted citation impact, top 2% 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

96 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.

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36 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 2 countries.

Mayuri ShuklaChulabhorn Graduate Institute, Chulabhorn Royal Academy, 54 Kamphaeng Phet 6 Road, Lak Si, Bangkok 10210. Thailand.
Piyarat GovitrapongChulabhorn Graduate Institute, Chulabhorn Royal Academy, Bangkok, 10210. Thailand.
Parichart BoontemChulabhorn Graduate Institute, Chulabhorn Royal Academy, 54 Kamphaeng Phet 6 Road, Lak Si, Bangkok 10210. Thailand.
Russel J ReiterDepartment of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, TX. United States.
Jutamaad SatayavivadChulabhorn Research Institute and Chulabhorn Graduate Institute, Chulabhorn Royal Academy, Bangkok 10210. Thailand.
Chulabhorn Graduate Institute · THThe University of Texas Health Science Center at San Antonio · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a chronic, progressive and prevalent neurodegenerative disease characterized by the loss of higher cognitive functions and an associated loss of memory. The thus far "incurable" stigma for AD prevails because of variations in the success rates of different treatment protocols in animal and human studies. Among the classical hypotheses explaining AD pathogenesis, the amyloid hypothesis is currently being targeted for drug development. The underlying concept is to prevent the formation of these neurotoxic peptides which play a central role in AD pathology and trigger a multispectral cascade of neurodegenerative processes post-aggregation. This could possibly be achieved by pharmacological inhibition of β- or γ-secretase or stimulating the nonamyloidogenic α-secretase. Melatonin the pineal hormone is a multifunctioning indoleamine. Production of this amphiphilic molecule diminishes with advancing age and this decrease runs parallel with the progression of AD which itself explains the potential benefits of melatonin in line of development and devastating consequences of the disease progression. Our recent studies have revealed a novel mechanism by which melatonin stimulates the nonamyloidogenic processing and inhibits the amyloidogenic processing of β-amyloid precursor protein (βAPP) by stimulating α -secretases and consequently down regulating both β- and γ-secretases at the transcriptional level. In this review, we discuss and evaluate the neuroprotective functions of melatonin in AD pathogenesis, including its role in the classical hypotheses in cellular and animal models and clinical interventions in AD patients, and suggest that with early detection, melatonin treatment is qualified to be an anti-AD therapy.

Indexed as

Alzheimer DiseaseAnimalsHumansMelatoninNeuroprotective AgentsMelatoninNeuroprotective AgentsagingAlzheimer's diseaseamyloid-β peptidemelatoninneuroprotection.secretases

Identifiers

PMID28294066
PMCPMC5652010
OpenAlexW2751493662

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.