Evidence map›Paper›PMID 34685563›Full record

ReviewCells2021

Inflammatory Cascade in Alzheimer's Disease Pathogenesis: A Review of Experimental Findings.

Jade de Oliveira, Ewa Kucharska, Michelle Lima Garcez, Matheus Scarpatto Rodrigues, João Quevedo, Ines Moreno-Gonzalez, Josiane Budni

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
7.2field-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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

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  13. Unraveling the oral microbiome's role in Alzheimer's disease: From pathophysiology to therapeutic potential.Alzheimer's & dementia : the journal of the Alzheimer's Association · 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

7 authors at 6 institutions in 4 countries.

Jade de OliveiraPrograma de Pós-Graduação em Ciências Biológicas: Bioquímica, Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre 90050-000, Brazil.ORCID 0000-0003-1454-2866
Ewa KucharskaFaculty of Education, Institute of Educational Sciences, Jesuit University Ignatianum in Krakow, 31-501 Krakow, Poland.
Michelle Lima GarcezDepartment of Biochemistry, Federal University of Santa Catarina, Florianópolis 88040-900, Santa Catarina, Brazil.
Matheus Scarpatto RodriguesPrograma de Pós-Graduação em Ciências Biológicas: Bioquímica, Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre 90050-000, Brazil.ORCID 0000-0002-7794-6588
João QuevedoTranslational Psychiatry Program, Faillace Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX 77030, USA.
Ines Moreno-GonzalezDepartment of Cell Biology, Faculty of Sciences, University of Malaga, IBIMA, 29010 Malaga, Spain.ORCID 0000-0003-3875-0889
Josiane BudniPrograma de Pós-Graduação em Ciências da Saúde, Laboratório de Neurologia Experimental, Universidade do Extremo Sul Catarinense, Criciuma 88806-000, Brazil.ORCID 0000-0003-4241-2743
Universidade Federal do Rio Grande do Sul · BRAkademia Ignatianum w Krakowie · PLBiomedical Research Networking Center on Neurodegenerative Diseases · ESThe University of Texas MD Anderson Cancer Center · USUniversidade do Extremo Sul Catarinense · BRUniversidade Federal de Santa Catarina · BR

Funding

Neural-derived extracellular vesicles microRNAs in bipolar disorder: a peripheral window into the brainR21MH117636 · NIMH · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI DE QUEVEDO, JOAO L · 2019 to 2020
$387k
Ministerio de Ciencia e Innovación PID2019-107090RA-I00Ministerio de Ciencia e Innovación RYC-2017-21879NIMH NIH HHS R21 MH117636
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the leading cause of dementia worldwide. Most AD patients develop the disease in late life, named late onset AD (LOAD). Currently, the most recognized explanation for AD pathology is the amyloid cascade hypothesis. It is assumed that amyloid beta (Aβ) aggregation and deposition are critical pathogenic processes in AD, leading to the formation of amyloid plaques, as well as neurofibrillary tangles, neuronal cell death, synaptic degeneration, and dementia. In LOAD, the causes of Aβ accumulation and neuronal loss are not completely clear. Importantly, the blood-brain barrier (BBB) disruption seems to present an essential role in the induction of neuroinflammation and consequent AD development. In addition, we propose that the systemic inflammation triggered by conditions like metabolic diseases or infections are causative factors of BBB disruption, coexistent inflammatory cascade and, ultimately, the neurodegeneration observed in AD. In this regard, the use of anti-inflammatory molecules could be an interesting strategy to treat, delay or even halt AD onset and progression. Herein, we review the inflammatory cascade and underlying mechanisms involved in AD pathogenesis and revise the anti-inflammatory effects of compounds as emerging therapeutic drugs against AD.

Indexed as

AgedAlzheimer DiseaseAnimalsDisease Models, AnimalFemaleHumansInflammationMaleMiceMice, TransgenicAlzheimer’s diseaseanti-inflammatory effectsBBB disruptiondementiainflammatory cascadeneurodegenerative diseaseneuroinflammationsystemic inflammationtherapy

Identifiers

PMID34685563
PMCPMC8533897
OpenAlexW3201982174

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.