Evidence map›Paper›PMID 36550479›Full record

ReviewBiological research2022

Inflammation context in Alzheimer's disease, a relationship intricate to define.

Catalina Novoa, Paulina Salazar, Pedro Cisternas, Camila Gherardelli, Roberto Vera-Salazar, Juan M Zolezzi, Nibaldo C Inestrosa

Open access · goldAbstract readReview
In one paragraph

Review in Biological research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed, 4 pooled it
17.8field-weighted citation impact, top 1% 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

117 citing papers in PubMed, 4 syntheses or guidelines pooled it, 169 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Review
  6. Holdfast-Derived Lipid Extract from the Patagonian MacroalgaPharmaceuticals (Basel, Switzerland) · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Inflammation profiles in Alzheimer's disease relate to cognition and neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. ZL006 Treatment Reduces Inflammation, Oxidative Stress, and Brain AβInternational journal of molecular sciences · 2026
    Article
  17. Review
  18. Article
  19. Article
  20. Article

57 more citing papers are in PubMed but not listed here.

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 4 institutions in 1 country.

Catalina Novoa *Centro de Envejecimiento y Regeneración (CARE-UC), Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda Bernardo O'Higgins 340, P.O. Box 114-D, Santiago, Chile.
Paulina Salazar *Centro de Envejecimiento y Regeneración (CARE-UC), Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda Bernardo O'Higgins 340, P.O. Box 114-D, Santiago, Chile.
Pedro CisternasInstituto de Ciencias de la Salud, Universidad de O'Higgins, Rancagua, Chile.
Camila GherardelliCentro de Envejecimiento y Regeneración (CARE-UC), Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda Bernardo O'Higgins 340, P.O. Box 114-D, Santiago, Chile.
Roberto Vera-SalazarFacultad de Ciencias Médicas, Escuela de Kinesiología, Universidad de Santiago de Chile, Santiago, Chile.
Juan M ZolezziCentro de Excelencia en Biomedicina de Magallanes (CEBIMA), Escuela de Medicina, Universidad de Magallanes, Punta Arenas, Chile.
Nibaldo C InestrosaCentro de Envejecimiento y Regeneración (CARE-UC), Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda Bernardo O'Higgins 340, P.O. Box 114-D, Santiago, Chile. ninestrosa@bio.puc.cl.
Pontificia Universidad Católica de Chile · CLUniversidad de Magallanes · CLUniversidad de Santiago de Chile · CLUniversity of O'Higgins · CL

Funding

FONIS EULACH16/T010131FONIS EULACH16/T010132
6 · The paper itself

Abstract

Alzheimer's disease (AD), the most common form of dementia, is characterized by the accumulation of amyloid β (Aβ) and hyperphosphorylated tau protein aggregates. Importantly, Aβ and tau species are able to activate astrocytes and microglia, which release several proinflammatory cytokines, such as tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β), together with reactive oxygen (ROS) and nitrogen species (RNS), triggering neuroinflammation. However, this inflammatory response has a dual function: it can play a protective role by increasing Aβ degradation and clearance, but it can also contribute to Aβ and tau overproduction and induce neurodegeneration and synaptic loss. Due to the significant role of inflammation in the pathogenesis of AD, several inflammatory mediators have been proposed as AD markers, such as TNF-α, IL-1β, Iba-1, GFAP, NF-κB, TLR2, and MHCII. Importantly, the use of anti-inflammatory drugs such as NSAIDs has emerged as a potential treatment against AD. Moreover, diseases related to systemic or local inflammation, including infections, cerebrovascular accidents, and obesity, have been proposed as risk factors for the development of AD. In the following review, we focus on key inflammatory processes associated with AD pathogenesis.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesHumansInflammationMicrogliaNF-kappa BTumor Necrosis Factor-alphaAmyloid beta-PeptidesNF-kappa BTumor Necrosis Factor-alpha

Identifiers

PMID36550479
PMCPMC9784299
OpenAlexW4312178155

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.