Evidence map›Paper›PMID 38832985›Full record

ReviewNaunyn-Schmiedeberg's archives of pharmacology2024

Oxidative stress-mediated neuroinflammation in Alzheimer's disease.

Sayed Mohammed Firdous, Sahabaj Ali Khan, Amritangshu Maity

Abstract readReview
PubMed Publisher
In one paragraph

Review in Naunyn-Schmiedeberg's archives of pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
–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

45 citing papers in PubMed.

  1. Article
  2. Therapeutic Effects ofMolecules (Basel, Switzerland) · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Immune-proteo-metabolomic changes link to Aβ and tau pathology in Alzheimer disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  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

3 authors.

Sayed Mohammed FirdousDepartment of Pharmacology, Calcutta Institute of Pharmaceutical Technology & AHS, Uluberia, Howrah, 711316, West Bengal, India. firdous.oncology@gmail.com.ORCID 0000-0003-4592-3880
Sahabaj Ali KhanDepartment of Pharmacology, Calcutta Institute of Pharmaceutical Technology & AHS, Uluberia, Howrah, 711316, West Bengal, India.ORCID 0000-0002-0515-3511
Amritangshu MaityDepartment of Pharmacology, Calcutta Institute of Pharmaceutical Technology & AHS, Uluberia, Howrah, 711316, West Bengal, India.ORCID 0009-0005-3138-3387

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reactive oxygen species (ROS) are metabolic by-products that constitute an indispensable component of physiological processes, albeit their heightened presence may proffer substantial perils to biological entities. Such a proliferation gives rise to a gradual escalation of oxidative stress within the organism, thereby compromising mitochondrial functionality and inflicting harm upon various bodily systems, with a particular predilection for the central nervous system. In its nascent stages, it is plausible that inflammation has been a facilitator in the progression of the malady. The precise role of inflammation in Alzheimer's disease (AD) remains somewhat enigmatic, although it is conceivable that activated microglia and astrocytes might be implicated in the removal of amyloid-β (Aβ) deposits. Nonetheless, prolonged microglial activation is associated with Tau phosphorylation and Aβ aggregation. Research studies have indicated that AD brains upregulate complementary molecules, inflammatory cytokines, acute phase reacting agents, and other inflammatory mediators that may cause neurodegeneration. In this review, oxidative damage products will be discussed as potential peripheral biomarkers for AD and its early stages. The disordered excretion of pro-inflammatory cytokines, chemokines, oxygen, and nitrogen-reactive species, along with the stimulation of the complement system by glial cells, has the potential to disrupt the functionality of neuronal termini. This perturbation, in turn, culminates in compromised synaptic function, a phenomenon empirically linked to the manifestation of cognitive impairments. The management of neurodegenerative conditions in the context of dementia necessitates therapeutic interventions that specifically target the excessive production of inflammatory and oxidative agents. Furthermore, we shall deliberate upon the function of microglia and oxidative injury in the etiology of AD and the ensuing neurodegenerative processes.

Indexed as

Alzheimer DiseaseNeuroinflammatory DiseasesOxidative StressAnimalsHumansInflammationReactive Oxygen SpeciesReactive Oxygen SpeciesAlzheimer’s diseaseBiomarkersNeurodegenerativeOxidative damageROS

Identifiers

PMID38832985

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.