Evidence map›Paper›PMID 37251647›Full record

ReviewFrontiers in molecular neuroscience2023

Is Drp1 a link between mitochondrial dysfunction and inflammation in Alzheimer's disease?

Oualid Sbai, Veronica Bazzani, Shreya Tapaswi, Joshua McHale, Carlo Vascotto, Lorena Perrone

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. DRP1, fission and apoptosis.Cell death discovery · 2025
    Review
  11. Article
  12. From Stress to Synapse: The Neuronal Atrophy Pathway to Mood Dysregulation.International journal of molecular sciences · 2025
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Mitochondria in Alzheimer's Disease Pathogenesis.Life (Basel, Switzerland) · 2024
    Review
  18. 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 4 institutions in 3 countries.

Oualid SbaiInstitut Pasteur de Tunis, LR11IPT02, Laboratory of Transmission, Control and Immunobiology of Infections (LTCII), Tunis, Tunisia.
Veronica BazzaniDepartment of Medicine, University of Udine, Udine, Italy.
Shreya TapaswiIMol Polish Academy of Sciences, Warsaw, Poland.
Joshua McHaleDepartment of Medicine, University of Udine, Udine, Italy.
Carlo VascottoDepartment of Medicine, University of Udine, Udine, Italy.
Lorena PerroneDepartment of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Naples, Italy.
University of Udine · ITInstitut Pasteur de Tunis · TNPolish Academy of Sciences · PLUniversity of Campania "Luigi Vanvitelli" · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent advances highlight that inflammation is critical to Alzheimer Disease (AD) pathogenesis. Indeed, several diseases characterized by inflammation are considered risk factors for AD, such as type 2 diabetes, obesity, hypertension, and traumatic brain injury. Moreover, allelic variations in genes involved in the inflammatory cascade are risk factors for AD. AD is also characterized by mitochondrial dysfunction, which affects the energy homeostasis of the brain. The role of mitochondrial dysfunction has been characterized mostly in neuronal cells. However, recent data are demonstrating that mitochondrial dysfunction occurs also in inflammatory cells, promoting inflammation and the secretion of pro-inflammatory cytokines, which in turn induce neurodegeneration. In this review, we summarize the recent finding supporting the hypothesis of the inflammatory-amyloid cascade in AD. Moreover, we describe the recent data that demonstrate the link between altered mitochondrial dysfunction and the inflammatory cascade. We focus in summarizing the role of Drp1, which is involved in mitochondrial fission, showing that altered Drp1 activation affects the mitochondrial homeostasis and leads to the activation of the NLRP3 inflammasome, promoting the inflammatory cascade, which in turn aggravates Amyloid beta (Ab) deposition and tau-induced neurodegeneration, showing the relevance of this pro-inflammatory pathway as an early event in AD.

Indexed as

Alzheimer inflammationDRP1mitochondriaNLRP3TXNIP

Identifiers

PMID37251647
PMCPMC10213291
OpenAlexW4376280119

What OpenQuestion 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 OpenQuestion graph.