Evidence map›Paper›PMID 34577590›Full record

ReviewPharmaceuticals (Basel, Switzerland)2021

Metformin a Potential Pharmacological Strategy in Late Onset Alzheimer's Disease Treatment.

Saghar Rabiei Poor, Miren Ettcheto, Amanda Cano, Elena Sanchez-Lopez, Patricia Regina Manzine, Jordi Olloquequi, Antoni Camins, Mohammad Javan

Open access · goldAbstract readReview
In one paragraph

Review in Pharmaceuticals (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
3.6field-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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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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

8 authors at 5 institutions in 4 countries.

Saghar Rabiei PoorDepartment of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran 14117-13116, Iran.
Miren EttchetoDepartment of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, Institut de Neurociències, University of Barcelona, 08028 Barcelona, Spain.ORCID 0000-0002-4301-7297
Amanda CanoBiomedical Research Networking Centre in Neurodegenerative Diseases (CIBERNED), 08028 Madrid, Spain.ORCID 0000-0001-9567-4283
Elena Sanchez-LopezBiomedical Research Networking Centre in Neurodegenerative Diseases (CIBERNED), 08028 Madrid, Spain.ORCID 0000-0003-2571-108X
Patricia Regina ManzineDepartment of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, Institut de Neurociències, University of Barcelona, 08028 Barcelona, Spain.ORCID 0000-0003-3460-9300
Jordi OlloquequiLaboratory of Cellular and Molecular Pathology, Institute of Biomedical Sciences, Faculty of Health Sciences, Universidad Autónoma de Chile, Talca 3467987, Chile.
Antoni CaminsDepartment of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, Institut de Neurociències, University of Barcelona, 08028 Barcelona, Spain.ORCID 0000-0002-1229-5956
Mohammad JavanDepartment of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran 14117-13116, Iran.ORCID 0000-0003-2045-6171
Biomedical Research Networking Center on Neurodegenerative Diseases · ESTarbiat Modares University · IRUniversidad Autónoma de Chile · CLUniversidade Federal de São Carlos · BRUniversitat Internacional de Catalunya · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is one of the most devastating brain disorders. Currently, there are no effective treatments to stop the disease progression and it is becoming a major public health concern. Several risk factors are involved in the progression of AD, modifying neuronal circuits and brain cognition, and eventually leading to neuronal death. Among them, obesity and type 2 diabetes mellitus (T2DM) have attracted increasing attention, since brain insulin resistance can contribute to neurodegeneration. Consequently, AD has been referred to "type 3 diabetes" and antidiabetic medications such as intranasal insulin, glitazones, metformin or liraglutide are being tested as possible alternatives. Metformin, a first line antihyperglycemic medication, is a 5'-adenosine monophosphate (AMP)-activated protein kinase (AMPK) activator hypothesized to act as a geroprotective agent. However, studies on its association with age-related cognitive decline have shown controversial results with positive and negative findings. In spite of this, metformin shows positive benefits such as anti-inflammatory effects, accelerated neurogenesis, strengthened memory, and prolonged life expectancy. Moreover, it has been recently demonstrated that metformin enhances synaptophysin, sirtuin-1, AMPK, and brain-derived neuronal factor (BDNF) immunoreactivity, which are essential markers of plasticity. The present review discusses the numerous studies which have explored (1) the neuropathological hallmarks of AD, (2) association of type 2 diabetes with AD, and (3) the potential therapeutic effects of metformin on AD and preclinical models.

Indexed as

Alzheimer’s diseaseAMP activated protein kinase (AMPK)beta amyloiddiabetes mellitusinsulin resistancemetformintau protein hyperphosphorylation

Identifiers

PMID34577590
PMCPMC8465337
OpenAlexW3198718085

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.