Evidence map›Paper›PMID 34834468›Full record

ReviewJournal of personalized medicine2021

Mechanisms Involved in Microglial-Interceded Alzheimer's Disease and Nanocarrier-Based Treatment Approaches.

Shadab Md, Nabil A Alhakamy, Mohamed A Alfaleh, Obaid Afzal, Abdulmalik S A Altamimi, Ashif Iqubal, Rasheed A Shaik

Open access · goldAbstract readReview
In one paragraph

Review in Journal of personalized medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Do Sleep Disturbances have a Dual Effect on Alzheimer's Disease?Cellular and molecular neurobiology · 2023
    Review
  11. Review
  12. Neuroinflammation: A Potential Risk for Dementia.International journal of molecular sciences · 2022
    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

7 authors at 3 institutions in 2 countries.

Shadab MdDepartment of Pharmaceutics, Faculty of Pharmacy, King Abdulaziz University, Jeddah 21589, Saudi Arabia.ORCID 0000-0002-9343-1066
Nabil A AlhakamyDepartment of Pharmaceutics, Faculty of Pharmacy, King Abdulaziz University, Jeddah 21589, Saudi Arabia.ORCID 0000-0002-3826-1519
Mohamed A AlfalehDepartment of Pharmaceutics, Faculty of Pharmacy, King Abdulaziz University, Jeddah 21589, Saudi Arabia.ORCID 0000-0003-3716-0019
Obaid AfzalDepartment of Pharmaceutical Chemistry, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al-Kharj 11942, Saudi Arabia.ORCID 0000-0002-4188-5592
Abdulmalik S A AltamimiDepartment of Pharmaceutical Chemistry, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al-Kharj 11942, Saudi Arabia.
Ashif IqubalDepartment of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi 110062, India.ORCID 0000-0003-4694-4851
Rasheed A ShaikDepartment of Pharmacology & Toxicology, Faculty of Pharmacy, King Abdulaziz University, Jeddah 21589, Saudi Arabia.
King Abdulaziz University · SAPrince Sattam Bin Abdulaziz University · SAJamia Hamdard · IN

Funding

King Abdulaziz University FP-031-43
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a common neurodegenerative disorder accountable for dementia and cognitive dysfunction. The etiology of AD is complex and multifactorial in origin. The formation and deposition of amyloid-beta (Aβ), hyperphosphorylated tau protein, neuroinflammation, persistent oxidative stress, and alteration in signaling pathways have been extensively explored among the various etiological hallmarks. However, more recently, the immunogenic regulation of AD has been identified, and macroglial activation is considered a limiting factor in its etiological cascade. Macroglial activation causes neuroinflammation via modulation of the NLRP3/NF-kB/p38 MAPKs pathway and is also involved in tau pathology via modulation of the GSK-3β/p38 MAPK pathways. Additionally, microglial activation contributes to the discrete release of neurotransmitters and an altered neuronal synaptic plasticity. Therefore, activated microglial cells appear to be an emerging target for managing and treating AD. This review article discussed the pathology of microglial activation in AD and the role of various nanocarrier-based anti-Alzeihmenr's therapeutic approaches that can either reverse or inhibit this activation. Thus, as a targeted drug delivery system, nanocarrier approaches could emerge as a novel means to overcome existing AD therapy limitations.

Indexed as

dementiaglial cellsimmunopathologynanocarriersneuroinflammationsignaling pathways

Identifiers

PMID34834468
PMCPMC8619529
OpenAlexW3211092327

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.