Evidence map›Paper›PMID 34069618›Full record

ReviewBiomedicines2021

Systemic Actions of SGLT2 Inhibition on Chronic mTOR Activation as a Shared Pathogenic Mechanism between Alzheimer's Disease and Diabetes.

Gabriela Dumitrita Stanciu, Razvan Nicolae Rusu, Veronica Bild, Leontina Elena Filipiuc, Bogdan-Ionel Tamba, Daniela Carmen Ababei

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 2 pooled it
3.7field-weighted citation impact, top 6% 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, 2 syntheses or guidelines pooled it, 46 citations in OpenAlex.

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  12. Blood Pressure Management Strategies and Podocyte Health.American journal of hypertension · 2025
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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

6 authors at 1 institution in 1 country.

Gabriela Dumitrita StanciuCenter for Advanced Research and Development in Experimental Medicine (CEMEX), Grigore T. Popa University of Medicine and Pharmacy, 16 Universitatii Street, 700115 Iasi, Romania.ORCID 0000-0003-4440-9628
Razvan Nicolae RusuPharmacodynamics and Clinical Pharmacy Department, Grigore T. Popa University of Medicine and Pharmacy, 16 Universitatii Street, 700115 Iasi, Romania.
Veronica BildCenter for Advanced Research and Development in Experimental Medicine (CEMEX), Grigore T. Popa University of Medicine and Pharmacy, 16 Universitatii Street, 700115 Iasi, Romania.
Leontina Elena FilipiucCenter for Advanced Research and Development in Experimental Medicine (CEMEX), Grigore T. Popa University of Medicine and Pharmacy, 16 Universitatii Street, 700115 Iasi, Romania.
Bogdan-Ionel TambaCenter for Advanced Research and Development in Experimental Medicine (CEMEX), Grigore T. Popa University of Medicine and Pharmacy, 16 Universitatii Street, 700115 Iasi, Romania.ORCID 0000-0001-9868-1999
Daniela Carmen AbabeiPharmacodynamics and Clinical Pharmacy Department, Grigore T. Popa University of Medicine and Pharmacy, 16 Universitatii Street, 700115 Iasi, Romania.
Grigore T. Popa University of Medicine and Pharmacy · RO

Funding

"Grigore T. Popa" University of Medicine and Pharmacy, Iasi Romania 4715/25.02.2021
6 · The paper itself

Abstract

Alzheimer's disease (AD) affects tens of millions of people worldwide. Despite the advances in understanding the disease, there is an increased urgency for pharmacological approaches able of impacting its onset and progression. With a multifactorial nature, high incidence and prevalence in later years of life, there is growing evidence highlighting a relationship between metabolic dysfunction related to diabetes and subject's susceptibility to develop AD. The link seems so solid that sometimes AD and type 3 diabetes are used interchangeably. A candidate for a shared pathogenic mechanism linking these conditions is chronically-activated mechanistic target of rapamycin (mTOR). Chronic activation of unrestrained mTOR could be responsible for sustaining metabolic dysfunction that causes the breakdown of the blood-brain barrier, tau hyperphosphorylation and senile plaques formation in AD. It has been suggested that inhibition of sodium glucose cotransporter 2 (SGLT2) mediated by constant glucose loss, may restore mTOR cycle via nutrient-driven, preventing or even decreasing the AD progression. Currently, there is an unmet need for further research insight into molecular mechanisms that drive the onset and AD advancement as well as an increase in efforts to expand the testing of potential therapeutic strategies aimed to counteract disease progression in order to structure effective therapies.

Indexed as

Alzheimer’s diseasediabetesmechanistic target of rapamycinmetabolic dysfunction hypothesissodium glucose cotransporter 2 inhibition

Identifiers

PMID34069618
PMCPMC8160780
OpenAlexW3161031064

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.