Evidence map›Paper›PMID 37511515›Full record

ReviewInternational journal of molecular sciences2023

The Molecular Mechanisms of Neuroinflammation in Alzheimer's Disease, the Consequence of Neural Cell Death.

Su-Bin Choi, Sehee Kwon, Ji-Hye Kim, Na-Hyun Ahn, Joo-Hee Lee, Seung-Hoon Yang

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 3 pooled it
7.8field-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

33 citing papers in PubMed, 3 syntheses or guidelines pooled it, 51 citations in OpenAlex.

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  17. Ameliorating potential ofFrontiers in nutrition · 2025
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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 1 institution in 1 country.

Su-Bin ChoiDepartment of Biomedical Engineering, College of Life Science and Biotechnology, Dongguk University, Seoul 04620, Republic of Korea.
Sehee KwonDepartment of Biomedical Engineering, College of Life Science and Biotechnology, Dongguk University, Seoul 04620, Republic of Korea.
Ji-Hye KimDepartment of Biomedical Engineering, College of Life Science and Biotechnology, Dongguk University, Seoul 04620, Republic of Korea.
Na-Hyun AhnDepartment of Biomedical Engineering, College of Life Science and Biotechnology, Dongguk University, Seoul 04620, Republic of Korea.
Joo-Hee LeeDepartment of Biomedical Engineering, College of Life Science and Biotechnology, Dongguk University, Seoul 04620, Republic of Korea.
Seung-Hoon YangDepartment of Biomedical Engineering, College of Life Science and Biotechnology, Dongguk University, Seoul 04620, Republic of Korea.ORCID 0000-0002-6880-8861
Dongguk University · KR

Funding

Korea Health Industry Development Institute HU21C0161National Research Foundation of Korea 2015R1A6A3A04058568National Research Foundation of Korea 2020R1F1A1076240National Research Foundation of Korea 2021R1C1C1009743
6 · The paper itself

Abstract

Alzheimer's disease (AD) is accompanied by neural cell loss and memory deficit. Neural cell death, occurring via apoptosis and autophagy, is widely observed in the AD brain in addition to neuroinflammation mediated by necroptosis and the NLRP3 inflammasome. Neurotoxicity induced by amyloid-beta (Aβ) and tau aggregates leads to excessive neural cell death and neuroinflammation in the AD brain. During AD progression, uncontrolled neural cell death results in the dysregulation of cellular activity and synaptic function. Apoptosis mediated by pro-apoptotic caspases, autophagy regulated by autophagy-related proteins, and necroptosis controlled by the RIPK/MLKL axis are representative of neural cell death occurred during AD. Necroptosis causes the release of cellular components, contributing to the pro-inflammatory environment in the AD brain. Inordinately high levels of neural cell death and pro-inflammatory events lead to the production of pro-inflammatory cytokines and feed-forward hyper neuroinflammation. Thus, neural cell death and neuroinflammation cause synaptic dysfunction and memory deficits in the AD brain. In this review, we briefly introduce the mechanisms of neural cell death and neuroinflammation observed in the AD brain. Combined with a typical strategy for targeting Aβ and tau, regulation of neural cell death and neuroinflammation may be effective for the amelioration of AD pathologies.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesCell DeathHumansInflammasomesNeuroinflammatory DiseasesAmyloid beta-PeptidesInflammasomesAlzheimer’s diseaseapoptosisautophagynecroptosisneural cell deathneuroinflammationNLRP3 inflammasome

Identifiers

PMID37511515
PMCPMC10380735
OpenAlexW4385224523

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.