Evidence map›Paper›PMID 30900203›Full record

ReviewCNS drugs2019

Targeting Inflammatory Pathways in Alzheimer's Disease: A Focus on Natural Products and Phytomedicines.

Matthew J Sharman, Giuseppe Verdile, Shanmugam Kirubakaran, Cristina Parenti, Ahilya Singh, Georgina Watt, Tim Karl, Dennis Chang, Chun Guang Li, Gerald Münch

Abstract readReview
PubMed Publisher
In one paragraph

Review in CNS drugs, 2019. 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
3.1field-weighted citation impact, top 8% 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, 35 citations in OpenAlex.

  1. Article
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  3. Review
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  10. Article
  11. Molecules (Basel, Switzerland) · 2022
    Article
  12. Review
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  15. Article
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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

10 authors at 4 institutions in 1 country.

Matthew J SharmanSchool of Health Sciences, College of Health and Medicine, University of Tasmania, Locked Bag 1322, Launceston, TAS, 7250, Australia.
Giuseppe VerdileSchool of Pharmacy and Biomedical Sciences, Curtin Health Innovation Research Institute, Curtin University, Bentley, WA, 6102, Australia.
Shanmugam KirubakaranDepartment of Pharmacology, School of Medicine, Western Sydney University, Campbelltown, NSW, 2560, Australia.
Cristina ParentiDepartment of Pharmacology, School of Medicine, Western Sydney University, Campbelltown, NSW, 2560, Australia.
Ahilya SinghDepartment of Pharmacology, School of Medicine, Western Sydney University, Campbelltown, NSW, 2560, Australia.
Georgina WattDepartment of Behavioural Neuroscience, School of Medicine, Western Sydney University, Campbelltown, NSW, 2560, Australia.
Tim KarlDepartment of Behavioural Neuroscience, School of Medicine, Western Sydney University, Campbelltown, NSW, 2560, Australia.
Dennis ChangNICM Health Research Institute, Western Sydney University, Campbelltown, NSW, 2560, Australia.
Chun Guang LiNICM Health Research Institute, Western Sydney University, Campbelltown, NSW, 2560, Australia.
Gerald MünchDepartment of Pharmacology, School of Medicine, Western Sydney University, Campbelltown, NSW, 2560, Australia. g.muench@westernsydney.edu.au.ORCID http://orcid.org/0000-0002-4873-7779
Camden and Campbelltown Hospitals · AUWestern Sydney University · AUCurtin University · AUUniversity of Tasmania · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies of the brains of Alzheimer's disease (AD) patients have revealed key neuropathological features, such as the deposition of aggregates of insoluble amyloid-β (Aβ) peptides and neurofibrillary tangles (NFTs). These pathological protein deposits, including Aβ peptides (which form senile plaques) and hyperphosphorylated tau (which aggregates into NFTs), have been assumed to be 'the cause of AD'. Aβ has been extensively targeted to develop an effective disease-modifying therapy, but with limited clinical success. Emerging therapies are also now targeting further pathological processes in AD, including neuroinflammation. This review focuses on the inflammatory and oxidative stress-related changes that occur in AD, and discusses some emerging anti-inflammatory natural products and phytomedicines. Many of the promising compounds are cytokine-suppressive anti-inflammatory drugs (CSAIDs), which target the proinflammatory AP1 and nuclear factor-κB signalling pathways and inhibit the expression of many proinflammatory cytokines, such as interleukin (IL)-1, IL-6, tumour necrosis factor-α, or nitric oxide produced by inducible nitric oxide synthase. However, many of these phytomedicines have not been tested in rigorous clinical trials in AD patients. It is not yet clear if the active compounds reach an effective concentration in the brain (due to limited bioavailability) or if they can slow down AD progression in long-term trials. The authors suggest that it is crucial for both the pharmacological and complementary medicine industries to conduct and fund those studies to significantly advance the field.

Indexed as

Alzheimer DiseaseAnti-Inflammatory AgentsBiological ProductsClinical Trials as TopicCytokinesGlycation End Products, AdvancedHumansInflammationNF-kappa BOxidative StressAnti-Inflammatory AgentsBiological ProductsCytokinesGlycation End Products, AdvancedNF-kappa B

Identifiers

PMID30900203
OpenAlexW2923619836

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.