Evidence map›Paper›PMID 35443732›Full record

ReviewAlzheimer's research & therapy2022

Glucose metabolism and AD: evidence for a potential diabetes type 3.

Andrea González, Camila Calfío, Macarena Churruca, Ricardo B Maccioni

Abstract readReview
In one paragraph

Review in Alzheimer's research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing 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

56 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Personalized prevention of neurodegenerative diseases: scoping review and evidence gap map.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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

4 authors.

Andrea GonzálezLaboratory of Neurosciences and Functional Medicine, International Center for Biomedicine (ICC), Avda. Vitacura 3568, D 511-512, Vitacura, Santiago, Chile.
Camila CalfíoLaboratory of Neurosciences and Functional Medicine, International Center for Biomedicine (ICC), Avda. Vitacura 3568, D 511-512, Vitacura, Santiago, Chile.
Macarena ChurrucaLaboratory of Neurosciences and Functional Medicine, International Center for Biomedicine (ICC), Avda. Vitacura 3568, D 511-512, Vitacura, Santiago, Chile.
Ricardo B MaccioniLaboratory of Neurosciences and Functional Medicine, International Center for Biomedicine (ICC), Avda. Vitacura 3568, D 511-512, Vitacura, Santiago, Chile. rmaccioni45@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer's disease is the most prevalent cause of dementia in the elderly. Neuronal death and synaptic dysfunctions are considered the main hallmarks of this disease. The latter could be directly associated to an impaired metabolism. In particular, glucose metabolism impairment has demonstrated to be a key regulatory element in the onset and progression of AD, which is why nowadays AD is considered the type 3 diabetes.

methodsWe provide a thread regarding the influence of glucose metabolism in AD from three different perspectives: (i) as a regulator of the energy source, (ii) through several metabolic alterations, such as insulin resistance, that modify peripheral signaling pathways that influence activation of the immune system (e.g., insulin resistance, diabetes, etc.), and (iii) as modulators of various key post-translational modifications for protein aggregation, for example, influence on tau hyperphosphorylation and other important modifications, which determine its self-aggregating behavior and hence Alzheimer's pathogenesis.

conclusionsIn this revision, we observed a 3 edge-action in which glucose metabolism impairment is acting in the progression of AD: as blockade of energy source (e.g., mitochondrial dysfunction), through metabolic dysregulation and post-translational modifications in key proteins, such as tau. Therefore, the latter would sustain the current hypothesis that AD is, in fact, the novel diabetes type 3.

Indexed as

Alzheimer DiseaseDiabetes MellitusInsulin ResistanceAgedGlucoseHumansSignal TransductionGlucoseAlzheimer’s diseaseER stressGlucose metabolism impairmentInsulin resistanceTau posttranslational modifications

Identifiers

PMID35443732
PMCPMC9022265

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.