Evidence map›Paper›PMID 19885299›Full record

ArticleJournal of diabetes science and technology2008

Alzheimer's disease is type 3 diabetes-evidence reviewed.

Suzanne M de la Monte, Jack R Wands

2 registry-linked trialsOpen access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of diabetes science and technology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 532 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
532citing papers in PubMed, 5 pooled it
8.6field-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.

NCT02271750 completednot on this mapstarted 2014, after this paper: background citation

A Study of Insulin-like Growth Factors and Other Neurotrophic Factors in the Cerebrospinal Fluid From Patients With Dementia

TypeobservationalSponsorUniversity of AarhusRan2014Enrolled120ConditionsDementiaArmslumbar puncture
NCT06391853 nawithdrawnnot on this mapstarted 2024, after this paper: background citation

Investigating Brain Insulin Resistance in Alzheimer Disease with Intra-Nasal Insulin Administration: a Multimodal Neuroimaging Study

TypeinterventionalSponsorErasme University HospitalRan2024 to 2026Enrolled0ConditionsAlzheimer Disease, Mild Cognitive ImpairmentArmsInsulin, Placebo
3 · Its place in the literature

Who cites it

532 citing papers in PubMed, 5 syntheses or guidelines pooled it, 1,109 citations in OpenAlex.

  1. The effect of GLP-1 receptor agonists on cognition in nondiabetic patients with mild cognitive impairment or alzheimer's disease: a meta-analysis of randomized controlled trials.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
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  11. Optimization and Metabolomic Profiling ofInternational journal of molecular sciences · 2026
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  16. Glycolysis-enhancing αAlzheimer's research & therapy · 2026
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472 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

2 authors at 1 institution in 1 country.

Suzanne M de la MonteDepartment of Pathology, Rhode Island Hospital and the Warren Alpert Medical School at Brown University, Providence, Rhode Island, USA. suzanne_delamonte_md@brown.edu
Jack R Wands
Rhode Island Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) has characteristic histopathological, molecular, and biochemical abnormalities, including cell loss; abundant neurofibrillary tangles; dystrophic neurites; amyloid precursor protein, amyloid-beta (APP-Abeta) deposits; increased activation of prodeath genes and signaling pathways; impaired energy metabolism; mitochondrial dysfunction; chronic oxidative stress; and DNA damage. Gaining a better understanding of AD pathogenesis will require a framework that mechanistically interlinks all these phenomena. Currently, there is a rapid growth in the literature pointing toward insulin deficiency and insulin resistance as mediators of AD-type neurodegeneration, but this surge of new information is riddled with conflicting and unresolved concepts regarding the potential contributions of type 2 diabetes mellitus (T2DM), metabolic syndrome, and obesity to AD pathogenesis. Herein, we review the evidence that (1) T2DM causes brain insulin resistance, oxidative stress, and cognitive impairment, but its aggregate effects fall far short of mimicking AD; (2) extensive disturbances in brain insulin and insulin-like growth factor (IGF) signaling mechanisms represent early and progressive abnormalities and could account for the majority of molecular, biochemical, and histopathological lesions in AD; (3) experimental brain diabetes produced by intracerebral administration of streptozotocin shares many features with AD, including cognitive impairment and disturbances in acetylcholine homeostasis; and (4) experimental brain diabetes is treatable with insulin sensitizer agents, i.e., drugs currently used to treat T2DM. We conclude that the term "type 3 diabetes" accurately reflects the fact that AD represents a form of diabetes that selectively involves the brain and has molecular and biochemical features that overlap with both type 1 diabetes mellitus and T2DM.

Indexed as

Alzheimer's diseasecentral nervous systemdiabetesinsulin gene expressioninsulin signaling

Identifiers

PMID19885299
PMCPMC2769828
OpenAlexW2135148756

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.