Evidence map›Paper›PMID 36499613›Full record

ReviewInternational journal of molecular sciences2022

Type 2 Diabetes Mellitus and Alzheimer's Disease: Shared Molecular Mechanisms and Potential Common Therapeutic Targets.

Rim Hamzé, Etienne Delangre, Stefania Tolu, Manon Moreau, Nathalie Janel, Danielle Bailbé, Jamileh Movassat

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2022. 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
15.3field-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

64 citing papers in PubMed, 138 citations in OpenAlex.

  1. New Genetic Associations Between Alzheimer's Disease and Its Key Risk Factors.Psychogeriatrics : the official journal of the Japanese Psychogeriatric Society · 2026
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4 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

7 authors at 1 institution in 1 country.

Rim HamzéTeam Biology and Pathology of the Endocrine Pancreas, Unité de Biologie Fonctionnelle et Adaptative, CNRS, Université Paris Cité, F-75013 Paris, France.ORCID 0000-0002-0052-087X
Etienne DelangreTeam Biology and Pathology of the Endocrine Pancreas, Unité de Biologie Fonctionnelle et Adaptative, CNRS, Université Paris Cité, F-75013 Paris, France.
Stefania ToluTeam Biology and Pathology of the Endocrine Pancreas, Unité de Biologie Fonctionnelle et Adaptative, CNRS, Université Paris Cité, F-75013 Paris, France.ORCID 0000-0002-0928-5810
Manon MoreauTeam Degenerative Process, Stress and Aging, Unité de Biologie Fonctionnelle et Adaptative, CNRS, Université Paris Cité, F-75013 Paris, France.
Nathalie JanelTeam Degenerative Process, Stress and Aging, Unité de Biologie Fonctionnelle et Adaptative, CNRS, Université Paris Cité, F-75013 Paris, France.
Danielle BailbéTeam Biology and Pathology of the Endocrine Pancreas, Unité de Biologie Fonctionnelle et Adaptative, CNRS, Université Paris Cité, F-75013 Paris, France.
Jamileh MovassatTeam Biology and Pathology of the Endocrine Pancreas, Unité de Biologie Fonctionnelle et Adaptative, CNRS, Université Paris Cité, F-75013 Paris, France.ORCID 0000-0002-0314-1525
Centre National de la Recherche Scientifique · FR

Funding

CNRS NAUniversité Paris Cité NA
6 · The paper itself

Abstract

The global prevalence of diabetes mellitus and Alzheimer's disease is increasing alarmingly with the aging of the population. Numerous epidemiological data suggest that there is a strong association between type 2 diabetes and an increased risk of dementia. These diseases are both degenerative and progressive and share common risk factors. The amyloid cascade plays a key role in the pathophysiology of Alzheimer's disease. The accumulation of amyloid beta peptides gradually leads to the hyperphosphorylation of tau proteins, which then form neurofibrillary tangles, resulting in neurodegeneration and cerebral atrophy. In Alzheimer's disease, apart from these processes, the alteration of glucose metabolism and insulin signaling in the brain seems to induce early neuronal loss and the impairment of synaptic plasticity, years before the clinical manifestation of the disease. The large amount of evidence on the existence of insulin resistance in the brain during Alzheimer's disease has led to the description of this disease as "type 3 diabetes". Available animal models have been valuable in the understanding of the relationships between type 2 diabetes and Alzheimer's disease, but to date, the mechanistical links are poorly understood. In this non-exhaustive review, we describe the main molecular mechanisms that may link these two diseases, with an emphasis on impaired insulin and IGF-1 signaling. We also focus on GSK3β and DYRK1A, markers of Alzheimer's disease, which are also closely associated with pancreatic β-cell dysfunction and type 2 diabetes, and thus may represent common therapeutic targets for both diseases.

Indexed as

Alzheimer DiseaseDiabetes Mellitus, Type 2Amyloid beta-PeptidesAnimalsBrainInsulintau ProteinsAmyloid beta-PeptidesInsulintau ProteinsAlzheimer’s diseaseAβ peptidediabetesDYRK1Aglycogen synthase kinase 3insulin deficiencyinsulin resistanceinsulin secretiontau

Identifiers

PMID36499613
PMCPMC9739879
OpenAlexW4311629917

What Socratic 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 Socratic graph.