Evidence map›Paper›PMID 34480263›Full record

ReviewPharmaceutical research2021

Cognitive Deficits in Type-1 Diabetes: Aspects of Glucose, Cerebrovascular and Amyloid Involvement.

Justin Pickering, Rachel Wong, Hani Al-Salami, Virginie Lam, Ryu Takechi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pharmaceutical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Thalamic Nuclei Atrophy in Type 1 Diabetes Mellitus Across Disease Duration.Journal of magnetic resonance imaging : JMRI · 2026
    Article
  2. Review
  3. Article
  4. 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

5 authors at 2 institutions in 1 country.

Justin PickeringSchool of Population Health, Faculty of Health Sciences, Curtin University, Perth, WA, 6845, Australia.
Rachel WongInstitute for Resilient Regions, University of Southern Queensland, Springfield Central, QLD, 4300, Australia.
Hani Al-SalamiCurtin Medical School, Faculty of Health Sciences, Curtin University, Perth, WA, 6845, Australia.
Virginie LamSchool of Population Health, Faculty of Health Sciences, Curtin University, Perth, WA, 6845, Australia.
Ryu TakechiSchool of Population Health, Faculty of Health Sciences, Curtin University, Perth, WA, 6845, Australia. R.Takechi@curtin.edu.au.ORCID http://orcid.org/0000-0001-6359-3382
Curtin University · AUUniversity of Southern Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The evidence shows that individuals with type-1 diabetes mellitus (T1DM) are at greater risk of accelerated cognitive impairment and dementia. Although, to date the mechanisms are largely unknown. An emerging body of literature indicates that dysfunction of cerebral neurovascular network and plasma dyshomeostasis of soluble amyloid-β in association with impaired lipid metabolism are central to the onset and progression of cognitive deficits and dementia. However, the latter has not been extensively considered in T1DM. Therefore, in this review, we summarised the literature concerning altered lipid metabolism and cerebrovascular function in T1DM as an implication for potential pathways leading to cognitive decline and dementia.

Indexed as

AmyloidAnimalsCerebrovascular DisordersCognitive DysfunctionDiabetes Mellitus, Type 1GlucoseHumansLipid MetabolismAmyloidGlucoseamyloid-betacerebrovascular dysfunctionhyperglycemiatype 1 diabetes

Identifiers

PMID34480263
OpenAlexW3196987921

What OpenQuestion holds

Textmetadata
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.