Evidence map›Paper›PMID 35741054›Full record

ReviewCells2022

New Insights into Neuroinflammation Involved in Pathogenic Mechanism of Alzheimer's Disease and Its Potential for Therapeutic Intervention.

Tiantian Li, Li Lu, Eloise Pember, Xinuo Li, Bocheng Zhang, Zheying Zhu

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
6.3field-weighted citation impact, top 2% 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

49 citing papers in PubMed, 101 citations in OpenAlex.

  1. Mechanisms, Biomarkers and Therapeutic Implications of Neuroinflammation in Alzheimer's Disease.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2026
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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

6 authors at 2 institutions in 2 countries.

Tiantian LiSchool of Pharmacy, The University of Nottingham, Nottingham NG7 2RD, UK.
Li LuSchool of Pharmacy, The University of Nottingham, Nottingham NG7 2RD, UK.ORCID 0000-0002-8956-8924
Eloise PemberSchool of Pharmacy, The University of Nottingham, Nottingham NG7 2RD, UK.
Xinuo LiSchool of Pharmacy, China Pharmaceutical University, Nanjing 211112, China.
Bocheng ZhangSchool of Pharmacy, The University of Nottingham, Nottingham NG7 2RD, UK.
Zheying ZhuSchool of Pharmacy, The University of Nottingham, Nottingham NG7 2RD, UK.ORCID 0000-0002-2135-3812
University of Nottingham · GBChina Pharmaceutical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common form of dementia, affecting more than 50 million people worldwide with an estimated increase to 139 million people by 2050. The exact pathogenic mechanisms of AD remain elusive, resulting in the fact that the current therapeutics solely focus on symptomatic management instead of preventative or curative strategies. The two most widely accepted pathogenic mechanisms of AD include the amyloid and tau hypotheses. However, it is evident that these hypotheses cannot fully explain neuronal degeneration shown in AD. Substantial evidence is growing for the vital role of neuroinflammation in AD pathology. The neuroinflammatory hypothesis provides a new, exciting lead in uncovering the underlying mechanisms contributing to AD. This review aims to highlight new insights into the role of neuroinflammation in the pathogenesis of AD, mainly including the involvement of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), nucleotide-binding oligomerization domain, leucine-rich repeat-containing protein 3 (NLRP3)/caspase-1 axis, triggering receptor expressed on myeloid cells 2 (TREM2) and cGAS-STING as key influencers in augmenting AD development. The inflammasomes related to the pathways of NF-κB, NLRP3, TREM2, and cGAS-STING as biomarkers of the neuroinflammation associated with AD, as well as an overview of novel AD treatments based on these biomarkers as potential drug targets reported in the literature or under clinical trials, are explored.

Indexed as

Alzheimer DiseaseBiomarkersHumansNeuroinflammatory DiseasesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinNucleotidyltransferasesBiomarkersNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinNucleotidyltransferasesAlzheimer’s diseasecGAS-STINGneuroinflammationNF-κBNLRP3TREM2

Identifiers

PMID35741054
PMCPMC9221885
OpenAlexW4282945740

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.