Evidence map›Paper›PMID 36776238›Full record

ArticleJournal of translational internal medicine2022

Aberrant Energy Metabolism in Alzheimer's Disease.

Linjie Yu, Jiali Jin, Yun Xu, Xiaolei Zhu

Abstract read
In one paragraph

Article in Journal of translational internal medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
–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

36 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Glycolysis-enhancing αAlzheimer's research & therapy · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review
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.

Linjie YuMedical School and The State Key Laboratory of Pharmaceutical Biotechnology, Department of Neurology, Drum Tower Hospital, Nanjing University, Nanjing 210008, Jiangsu Province, China.
Jiali JinMedical School and The State Key Laboratory of Pharmaceutical Biotechnology, Department of Neurology, Drum Tower Hospital, Nanjing University, Nanjing 210008, Jiangsu Province, China.
Yun XuMedical School and The State Key Laboratory of Pharmaceutical Biotechnology, Department of Neurology, Drum Tower Hospital, Nanjing University, Nanjing 210008, Jiangsu Province, China.
Xiaolei ZhuMedical School and The State Key Laboratory of Pharmaceutical Biotechnology, Department of Neurology, Drum Tower Hospital, Nanjing University, Nanjing 210008, Jiangsu Province, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To maintain energy supply to the brain, a direct energy source called adenosine triphosphate (ATP) is produced by oxidative phosphorylation and aerobic glycolysis of glucose in the mitochondria and cytoplasm. Brain glucose metabolism is reduced in many neurodegenerative diseases, including Alzheimer's disease (AD), where it appears presymptomatically in a progressive and region-specific manner. Following dysregulation of energy metabolism in AD, many cellular repair/regenerative processes are activated to conserve the energy required for cell viability. Glucose metabolism plays an important role in the pathology of AD and is closely associated with the tricarboxylic acid cycle, type 2 diabetes mellitus, and insulin resistance. The glucose intake in neurons is from endothelial cells, astrocytes, and microglia. Damage to neurocentric glucose also damages the energy transport systems in AD. Gut microbiota is necessary to modulate bidirectional communication between the gastrointestinal tract and brain. Gut microbiota may influence the process of AD by regulating the immune system and maintaining the integrity of the intestinal barrier. Furthermore, some therapeutic strategies have shown promising therapeutic effects in the treatment of AD at different stages, including the use of antidiabetic drugs, rescuing mitochondrial dysfunction, and epigenetic and dietary intervention. This review discusses the underlying mechanisms of alterations in energy metabolism in AD and provides potential therapeutic strategies in the treatment of AD.

Indexed as

Alzheimer’s diseaseenergy metabolismgut–brain axisnerve cells

Identifiers

PMID36776238
PMCPMC9901551

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.