Evidence map›Paper›PMID 26442696›Full record

ReviewTrends in neurosciences2015

Microglial malfunction: the third rail in the development of Alzheimer's disease.

Siddhita D Mhatre, Connie A Tsai, Amanda J Rubin, Michelle L James, Katrin I Andreasson

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Trends in neurosciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

79 citing papers in PubMed, 139 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Decoding Alzheimer's Disease One Cell Class at a Time.Cellular and molecular neurobiology · 2026
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. CARD9 attenuates Aβ pathology and modifies microglial responses in an Alzheimer's disease mouse model.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article

19 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

5 authors at 2 institutions in 1 country.

Siddhita D MhatreDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA; Stanford Neurosciences Institute, Stanford, CA, USA.
Connie A TsaiDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA; Stanford Neurosciences Institute, Stanford, CA, USA; Neurosciences Graduate Program, Stanford University, Stanford, CA, USA.
Amanda J RubinDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA; Stanford Neurosciences Institute, Stanford, CA, USA; Neurosciences Graduate Program, Stanford University, Stanford, CA, USA.
Michelle L JamesDepartment of Radiology, Stanford University School of Medicine, Stanford, CA, USA.
Katrin I AndreassonDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA; Stanford Neurosciences Institute, Stanford, CA, USA. Electronic address: kandreas@stanford.edu.
Stanford University · USNeurosciences Institute · US

Funding

Training Program in Basic NeuroscienceT32MH020016 · NIMH · STANFORD UNIVERSITY · PI Justin L Gardner, Merritt C Maduke · 1997 to 2026
$16.2M
Prostanoid signaling and inflammation in aging and Alzheimer's diseaseR01AG030209 · NIA · STANFORD UNIVERSITY · PI ANDREASSON, KATRIN I. · 2009 to 2013
$1.6M
MODELS OF ALZHEIMER'S DISEASER01AG015799 · NIA · JOHNS HOPKINS UNIVERSITY · PI ANDREASSON, KATRIN I · 2000 to 2003
$982k
Validation of the PGE2 EP4 receptor as a therapeutic target in ADR21AG033914 · NIA · STANFORD UNIVERSITY · PI ANDREASSON, KATRIN I. · 2009 to 2010
$892k
NIA NIH HHS AG030209NIA NIH HHS AG033914NIA NIH HHS AG15799NIA NIH HHS R01 AG030209NIA NIH HHS R21 AG033914NIMH NIH HHS T32 MH020016
6 · The paper itself

Abstract

Studies of Alzheimer's disease (AD) have predominantly focused on two major pathologies: amyloid-β (Aβ) and hyperphosphorylated tau. These misfolded proteins can accumulate asymptomatically in distinct regions over decades. However, significant Aβ accumulation can be seen in individuals who do not develop dementia, and tau pathology limited to the transentorhinal cortex, which can appear early in adulthood, is usually clinically silent. Thus, an interaction between these pathologies appears to be necessary to initiate and propel disease forward to widespread circuits. Recent multidisciplinary findings strongly suggest that the third factor required for disease progression is an aberrant microglial immune response. This response may initially be beneficial; however, a maladaptive microglial response eventually develops, fueling a feed-forward spread of tau and Aβ pathology.

Indexed as

Alzheimer DiseaseAnimalsBrainHumansMicrogliaAlzheimer's diseaseAβ peptideBraak stagesepigenomicsGWASmicrogliatau phosphorylationtranscriptomics

Identifiers

PMID26442696
PMCPMC4670239
OpenAlexW2107986249

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.