Evidence map›Paper›PMID 33228179›Full record

ReviewInternational journal of molecular sciences2020

Can We Treat Neuroinflammation in Alzheimer's Disease?

Sandra Sánchez-Sarasúa, Iván Fernández-Pérez, Verónica Espinosa-Fernández, Ana María Sánchez-Pérez, Juan Carlos Ledesma

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
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

27 citing papers in PubMed.

  1. Review
  2. Article
  3. Beyond epilepsy: The expanding role of valproic acid in Alzheimer disease therapy - a review.The Journal of pharmacology and experimental therapeutics · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. CX3CL1 Derived from Bone Marrow Mesenchymal Stem Cells Inhibits AComputational and mathematical methods in medicine · 2022
    Article
  18. Review
  19. Review
  20. Review
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

5 authors.

Sandra Sánchez-SarasúaNeurobiotechnology Group, Department of Medicine, Health Science Faculty, Universitat Jaume I, 12071 Castellón, Spain.
Iván Fernández-PérezNeurobiotechnology Group, Department of Medicine, Health Science Faculty, Universitat Jaume I, 12071 Castellón, Spain.
Verónica Espinosa-FernándezNeurobiotechnology Group, Department of Medicine, Health Science Faculty, Universitat Jaume I, 12071 Castellón, Spain.ORCID 0000-0003-3818-2754
Ana María Sánchez-PérezNeurobiotechnology Group, Department of Medicine, Health Science Faculty, Universitat Jaume I, 12071 Castellón, Spain.
Juan Carlos LedesmaNeurobiotechnology Group, Department of Medicine, Health Science Faculty, Universitat Jaume I, 12071 Castellón, Spain.ORCID 0000-0001-6372-2842

Funding

Fundación Alicia Koplowitz G-83837286
6 · The paper itself

Abstract

Alzheimer's disease (AD), considered the most common type of dementia, is characterized by a progressive loss of memory, visuospatial, language and complex cognitive abilities. In addition, patients often show comorbid depression and aggressiveness. Aging is the major factor contributing to AD; however, the initial cause that triggers the disease is yet unknown. Scientific evidence demonstrates that AD, especially the late onset of AD, is not the result of a single event, but rather it appears because of a combination of risk elements with the lack of protective ones. A major risk factor underlying the disease is neuroinflammation, which can be activated by different situations, including chronic pathogenic infections, prolonged stress and metabolic syndrome. Consequently, many therapeutic strategies against AD have been designed to reduce neuro-inflammation, with very promising results improving cognitive function in preclinical models of the disease. The literature is massive; thus, in this review we will revise the translational evidence of these early strategies focusing in anti-diabetic and anti-inflammatory molecules and discuss their therapeutic application in humans. Furthermore, we review the preclinical and clinical data of nutraceutical application against AD symptoms. Finally, we introduce new players underlying neuroinflammation in AD: the activity of the endocannabinoid system and the intestinal microbiota as neuroprotectors. This review highlights the importance of a broad multimodal approach to treat successfully the neuroinflammation underlying AD.

Indexed as

AgingAlzheimer DiseaseAnti-Inflammatory AgentsCannabinoidsClinical Trials as TopicCognitive DysfunctionDepressionDietary SupplementsGastrointestinal MicrobiomeHumansHypoglycemic AgentsInflammationInsulin ResistanceMetabolic SyndromeNeuroimmunomodulationNeuroprotective AgentsAnti-Inflammatory AgentsCannabinoidsHypoglycemic AgentsNeuroprotective AgentsAlzheimer’s diseaseendocannabinoid systemgut microbiotainsulin resistanceneuroinflammationnutraceuticals

Identifiers

PMID33228179
PMCPMC7699542

What OpenQuestion holds

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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.