Evidence map›Paper›PMID 33358332›Full record

ReviewChinese journal of traumatology = Zhonghua chuang shang za zhi2021

Glucose metabolism: A link between traumatic brain injury and Alzheimer's disease.

Xiao-Jian Xu, Meng-Shi Yang, Bin Zhang, Fei Niu, Jin-Qian Dong, Bai-Yun Liu

Open access · diamondAbstract readReview
In one paragraph

Review in Chinese journal of traumatology = Zhonghua chuang shang za zhi, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 55 citations in OpenAlex.

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  5. Impact Induces Phagocytic Defect in Reactive Microglia.bioRxiv : the preprint server for biology · 2025
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  20. Association of life-course traumatic brain injury with dementia risk: A nationwide twin study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    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

6 authors at 3 institutions in 1 country.

Xiao-Jian XuBeijing Key Laboratory of Central Nervous System Injury, Beijing Neurosurgical Institute, Capital Medical University, Beijing, 100070, China.
Meng-Shi YangBeijing Key Laboratory of Central Nervous System Injury and Department of Neurosurgery, Beijing Neurosurgical Institute and Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Bin ZhangBeijing Key Laboratory of Central Nervous System Injury and Department of Neurosurgery, Beijing Neurosurgical Institute and Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Fei NiuBeijing Key Laboratory of Central Nervous System Injury, Beijing Neurosurgical Institute, Capital Medical University, Beijing, 100070, China.
Jin-Qian DongBeijing Key Laboratory of Central Nervous System Injury and Department of Neurosurgery, Beijing Neurosurgical Institute and Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China.
Bai-Yun LiuBeijing Key Laboratory of Central Nervous System Injury, Beijing Neurosurgical Institute, Capital Medical University, Beijing, 100070, China; Beijing Key Laboratory of Central Nervous System Injury and Department of Neurosurgery, Beijing Neurosurgical Institute and Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China; Nerve Injury and Repair Center of Beijing Institute for Brain Disorders, Beijing, 100070, China; China National Clinical Research Center for Neurological Diseases, Beijing, 100070, China. Electronic address: liubaiyun1212@163.com.
Capital Medical University · CNBeijing Institute of Neurosurgery · CNNational Clinical Research Center for Digestive Diseases · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI), a growing public health problem, is a leading cause of death and disability worldwide, although its prevention measures and clinical cares are substantially improved. Increasing evidence shows that TBI may increase the risk of mood disorders and neurodegenerative diseases, including Alzheimer's disease (AD). However, the complex relationship between TBI and AD remains elusive. Metabolic dysfunction has been the common pathology in both TBI and AD. On the one hand, TBI perturbs the glucose metabolism of the brain, and causes energy crisis and subsequent hyperglycolysis. On the other hand, glucose deprivation promotes amyloidogenesis via β-site APP cleaving enzyme-1 dependent mechanism, and triggers tau pathology and synaptic function. Recent findings suggest that TBI might facilitate Alzheimer's pathogenesis by altering metabolism, which provides clues to metabolic link between TBI and AD. In this review, we will explore how TBI-induced metabolic changes contribute to the development of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorBrainBrain Injuries, TraumaticGlucoseGlycolysisHumansTauopathiesAmyloid beta-Protein PrecursorGlucoseAlzheimer’s diseaseGlucose metabolismNeurological disorderTraumatic brain injury

Identifiers

PMID33358332
PMCPMC7878452
OpenAlexW3096059723

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.