Evidence map›Paper›PMID 37396164›Full record

ReviewFrontiers in endocrinology2023

Cognitive dysfunction in diabetes: abnormal glucose metabolic regulation in the brain.

Shan Zhang, Yueying Zhang, Zhige Wen, YaNan Yang, Tianjie Bu, Xiangwei Bu, Qing Ni

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

Review in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 3 pooled it
11.1field-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

67 citing papers in PubMed, 3 syntheses or guidelines pooled it, 90 citations in OpenAlex.

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7 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.

Shan ZhangDepartment of Endocrinology, Guang' anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Yueying ZhangDepartment of Endocrinology, Guang' anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Zhige WenDepartment of Endocrinology, Guang' anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
YaNan YangDepartment of Endocrinology, Guang' anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Tianjie BuDepartment of Endocrinology, Guang' anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Xiangwei BuDepartment of Endocrinology, Guang' anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Qing NiDepartment of Endocrinology, Guang' anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cognitive dysfunction is increasingly recognized as a complication and comorbidity of diabetes, supported by evidence of abnormal brain structure and function. Although few mechanistic metabolic studies have shown clear pathophysiological links between diabetes and cognitive dysfunction, there are several plausible ways in which this connection may occur. Since, brain functions require a constant supply of glucose as an energy source, the brain may be more susceptible to abnormalities in glucose metabolism. Glucose metabolic abnormalities under diabetic conditions may play an important role in cognitive dysfunction by affecting glucose transport and reducing glucose metabolism. These changes, along with oxidative stress, inflammation, mitochondrial dysfunction, and other factors, can affect synaptic transmission, neural plasticity, and ultimately lead to impaired neuronal and cognitive function. Insulin signal triggers intracellular signal transduction that regulates glucose transport and metabolism. Insulin resistance, one hallmark of diabetes, has also been linked with impaired cerebral glucose metabolism in the brain. In this review, we conclude that glucose metabolic abnormalities play a critical role in the pathophysiological alterations underlying diabetic cognitive dysfunction (DCD), which is associated with multiple pathogenic factors such as oxidative stress, mitochondrial dysfunction, inflammation, and others. Brain insulin resistance is highly emphasized and characterized as an important pathogenic mechanism in the DCD.

Indexed as

Cognitive DysfunctionDiabetes MellitusInsulin ResistanceBrainGlucoseHumansInflammationGlucosecerebral glucose metabolismcognitive dysfunctiondiabetesinsulin signalmolecular mechanism

Identifiers

PMID37396164
PMCPMC10312370
OpenAlexW4380991902

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.