Evidence map›Paper›PMID 35286658›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2022

Microglia in Alzheimer's Disease: a Key Player in the Transition Between Homeostasis and Pathogenesis.

Karen N McFarland, Paramita Chakrabarty

Open access · bronzeAbstract readReview
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. PreoperativeFrontiers in bioinformatics · 2026
    Review
  10. Review
  11. Article
  12. Review
  13. Modulatory Effects ofAntioxidants (Basel, Switzerland) · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. The brain pathobiome in Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    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

2 authors at 1 institution in 1 country.

Karen N McFarlandDepartment of Neurology, University of Florida, Gainesville, FL, 32610, USA.
Paramita ChakrabartyDepartment of Neuroscience, University of Florida, Gainesville, FL, 32610, USA. pchakrabarty@ufl.edu.ORCID 0000-0002-6226-3776
University of Florida · US

Funding

Social Determinants of Health, Race/Ethnicity, and White Matter HyperintensitiesP30AG066506 · NIA · UNIVERSITY OF FLORIDA · PI Rosie E Curiel Cid · 2020 to 2026
$25.6M
Elucidating factors that modulate tauopathy and cellular degeneration to guide therapeutic developmentRF1AG064914 · NIA · UNIVERSITY OF FLORIDA · PI GOLDE, TODD E, LEWIS, JADA M · 2019 to 2019
$2.5M
NIA NIH HHS P30 AG066506NIA NIH HHS RF1 AG064914
6 · The paper itself

Abstract

Immune activation accompanies the development of proteinopathy in the brains of Alzheimer's dementia patients. Evolving from the long-held viewpoint that immune activation triggers the pathological trajectory in Alzheimer's disease, there is accumulating evidence now that microglial activation is neither pro-amyloidogenic nor just a simple reactive process to the proteinopathy. Preclinical studies highlight an interesting aspect of immunity, i.e., spurring immune system activity may be beneficial under certain circumstances. Indeed, a dynamic evolving relationship between different activation states of the immune system and its neuronal neighbors is thought to regulate overall brain organ health in both healthy aging and progression of Alzheimer's dementia. A new premise evolving from genome, transcriptome, and proteome data is that there might be at least two major phases of immune activation that accompany the pathological trajectory in Alzheimer's disease. Though activation on a chronic scale will certainly lead to neurodegeneration, this emerging knowledge of a potential beneficial aspect of immune activation allows us to form holistic insights into when, where, and how much immune system activity would need to be tuned to impact the Alzheimer's neurodegenerative cascade. Even with the trove of recently emerging -omics data from patients and preclinical models, how microglial phenotypes are functionally related to the transition of a healthy aging brain towards progressive degenerative state remains unknown. A deeper understanding of the synergism between microglial functional states and brain organ health could help us discover newer interventions and therapies that enable us to address the current paucity of disease-modifying therapies in Alzheimer's disease.

Indexed as

Alzheimer DiseaseBrainHomeostasisHumansMicrogliaNeuronsAmyloid cascadeGene variantsImmunityNeurodegenerationProteomeTauTranscriptome

Identifiers

PMID35286658
PMCPMC9130399
OpenAlexW4221004276

What OpenQuestion holds

Textmetadata
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.