Evidence map›Paper›PMID 20205644›Full record

ReviewCNS & neurological disorders drug targets2010

Microglia and inflammation in Alzheimer's disease.

Shweta Mandrekar-Colucci, Gary E Landreth

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in CNS & neurological disorders drug targets, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 239 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
239citing papers in PubMed, 2 pooled it
12.3field-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

239 citing papers in PubMed, 2 syntheses or guidelines pooled it, 427 citations in OpenAlex.

  1. Pooled it
  2. COVID-19 associated cognitive impairment: A systematic review.Cortex; a journal devoted to the study of the nervous system and behavior · 2022
    Pooled it
  3. Article
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  6. Review
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  8. Review
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  10. Article
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  13. Rebalancing Immune Interactions within the Brain-Spleen Axis Mitigates Neuroinflammation in an Aging Mouse Model of Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  14. Review
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  20. Review

179 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

2 authors at 2 institutions in 1 country.

Shweta Mandrekar-ColucciDepartment of Neurosciences, Case Western Reserve University, Cleveland, OH 44106, USA.
Gary E Landreth
Case Comprehensive Cancer CenterCase Western Reserve University · US

Funding

MICROGLIAL SIGNALING MECHANISMS IN ALZHEIMER'S DISEASER01AG016740 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI LANDRETH, GARY E. · 2000 to 2010
$2.9M
LXR and PPARgamma mediated Abeta clearance mechanismsR01AG030482 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI LANDRETH, GARY E. · 2007 to 2011
$1.9M
The Role of PPARgamma Activation in the Proteolytic Clearance of AbetaF31NS061445 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI MANDREKAR, SHWETA · 2008 to 2009
$53k
NIA NIH HHS AG16740NIA NIH HHS R01 AG016740NIA NIH HHS R01 AG030482NINDS NIH HHS F31 NS061445
6 · The paper itself

Abstract

One hundred and fifty years have elapsed since the original discovery of the microglial cell by Virchow. While this cell type has been well studied, the role of microglia in the pathology of many central nervous system diseases still remains enigmatic. It is widely accepted that microglial-mediated inflammation contributes to the progression of Alzheimer's disease (AD); however, the precise mechanisms through which these cells contribute to AD-related inflammation remains to be elucidated. In the AD brain, microglial cells are found in close association with amyloid beta (Abeta) deposits. Histological examination of AD brains as well as cell culture studies have shown that the interaction of microglia with fibrillar Abeta leads to their phenotypic activation. The conversion of these cells into a classically 'activated' phenotype results in production of chemokines, neurotoxic cytokines and reactive oxygen and nitrogen species that are deleterious to the CNS. However, microglia also exert a neuroprotective role through their ability to phagocytose Abeta particles and clear soluble forms of Abeta. These cells have been documented to play integral roles in tissue repair and inflammation, and in recent years it has been appreciated that this cell type is capable of facilitating a more complex response to pathogens by changing their activation status. A variety of new findings indicate that their role in the central nervous system is far more complex than previously appreciated. In this review we discuss the role of microglia in the normal brain and their phenotypic heterogeneity and how this may play a role in AD-related pathophysiology. We touch on what is known about their ability to recognize and clear Abeta peptides as well as more controversial topics, including various activation states of microglia and the ability of peripheral macrophages or monocytes to infiltrate the brain.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainCytokinesEncephalitisGliosisHumansInflammation MediatorsMicrogliaAmyloid beta-PeptidesCytokinesInflammation Mediators

Identifiers

PMID20205644
PMCPMC3653290
OpenAlexW2024816116

What OpenQuestion holds

Textmetadata
LicenceTDM
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.