Evidence map›Paper›PMID 33066368›Full record

ReviewBiomolecules2020

Microglia in Alzheimer's Disease in the Context of Tau Pathology.

Juan Ramón Perea, Marta Bolós, Jesús Avila

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 109 citations in OpenAlex.

  1. Article
  2. Article
  3. Epigenetic aging in Alzheimer's disease: Relation to proteome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  4. Review
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  6. Article
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  10. Choroidal-ventricular system abnormalities are linked to amyloid-β aggregation in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
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  18. Article
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  20. Review

7 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

3 authors at 1 institution in 1 country.

Juan Ramón PereaDepartment of Molecular Neuropathology, Centro de Biología Molecular "Severo Ochoa" (CSIC-UAM), 1 Nicolás Cabrera, 28049 Madrid, Spain.ORCID 0000-0001-7607-8814
Marta BolósDepartment of Molecular Neuropathology, Centro de Biología Molecular "Severo Ochoa" (CSIC-UAM), 1 Nicolás Cabrera, 28049 Madrid, Spain.
Jesús AvilaDepartment of Molecular Neuropathology, Centro de Biología Molecular "Severo Ochoa" (CSIC-UAM), 1 Nicolás Cabrera, 28049 Madrid, Spain.ORCID 0000-0002-6288-0571
Biomedical Research Networking Center on Neurodegenerative Diseases · ES

Funding

Banco Santander Centro de Biología Molecular "Severo Ochoa"Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas Jesús ÁvilaFundación Ramón Areces Centro de Biología Molecular "Severo Ochoa"Ministerio de Ciencia e Innovación PGC2018-096177-B-00
6 · The paper itself

Abstract

Microglia are the cells that comprise the innate immune system in the brain. First described more than a century ago, these cells were initially assigned a secondary role in the central nervous system (CNS) with respect to the protagonists, neurons. However, the latest advances have revealed the complexity and importance of microglia in neurodegenerative conditions such as Alzheimer's disease (AD), the most common form of dementia associated with aging. This pathology is characterized by the accumulation of amyloid-β peptide (Aβ), which forms senile plaques in the neocortex, as well as by the aggregation of hyperphosphorylated tau protein, a process that leads to the development of neurofibrillary tangles (NFTs). Over the past few years, efforts have been focused on studying the interaction between Aβ and microglia, together with the ability of the latter to decrease the levels of this peptide. Given that most clinical trials following this strategy have failed, current endeavors focus on deciphering the molecular mechanisms that trigger the tau-induced inflammatory response of microglia. In this review, we summarize the most recent studies on the physiological and pathological functions of tau protein and microglia. In addition, we analyze the impact of microglial AD-risk genes (

Indexed as

AgingAlzheimer DiseaseAmyloid beta-PeptidesAnimalsHumansMicrogliaNeuritisProtein Aggregation, PathologicalTauopathiestau ProteinsAmyloid beta-Peptidestau ProteinsAlzheimer’s diseaseApoEAβCD33CX3CR1microglianeuroinflammationtautauopathiesTREM2

Identifiers

PMID33066368
PMCPMC7602223
OpenAlexW3093381072

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.