Evidence map›Paper›PMID 26001591›Full record

ArticleActa neuropathologica communications2015

Disease-related microglia heterogeneity in the hippocampus of Alzheimer's disease, dementia with Lewy bodies, and hippocampal sclerosis of aging.

Adam D Bachstetter, Linda J Van Eldik, Frederick A Schmitt, Janna H Neltner, Eseosa T Ighodaro, Scott J Webster, Ela Patel, Erin L Abner, Richard J Kryscio, Peter T Nelson

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
168citing papers in PubMed, 2 pooled it
11.2field-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

168 citing papers in PubMed, 2 syntheses or guidelines pooled it, 261 citations in OpenAlex.

  1. Pooled it
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  10. Where do PDD and DLB SYNdromes fit in neuronal alpha-SYNuclein biological frameworks?Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
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  15. A hypothesis explaining Alzheimer's disease, Parkinson's disease, and dementia with Lewy bodies overlap.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
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108 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

10 authors at 1 institution in 1 country.

Adam D BachstetterSanders-Brown Center on Aging, University of Kentucky, 800 S. Limestone St, Lexington, KY, USA. adam.bachstetter@uky.edu.
Linda J Van EldikSanders-Brown Center on Aging, University of Kentucky, 800 S. Limestone St, Lexington, KY, USA.
Frederick A SchmittSanders-Brown Center on Aging, University of Kentucky, 800 S. Limestone St, Lexington, KY, USA.
Janna H NeltnerSanders-Brown Center on Aging, University of Kentucky, 800 S. Limestone St, Lexington, KY, USA.
Eseosa T IghodaroSanders-Brown Center on Aging, University of Kentucky, 800 S. Limestone St, Lexington, KY, USA.
Scott J WebsterSanders-Brown Center on Aging, University of Kentucky, 800 S. Limestone St, Lexington, KY, USA.
Ela PatelSanders-Brown Center on Aging, University of Kentucky, 800 S. Limestone St, Lexington, KY, USA.
Erin L AbnerSanders-Brown Center on Aging, University of Kentucky, 800 S. Limestone St, Lexington, KY, USA.
Richard J KryscioDepartment of Biostatistics, University of Kentucky, Lexington, KY, USA.
Peter T NelsonSanders-Brown Center on Aging, University of Kentucky, 800 S. Limestone St, Lexington, KY, USA.
University of Kentucky · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI Jennifer F Rogers · 2013 to 2026
$38.3M
University of Kentucky Alzheimer's Disease Core Center - Biomarker CoreP30AG028383 · NIA · UNIVERSITY OF KENTUCKY · PI GOLD, BRIAN TIMOTHY, VAN ELDIK, LINDA J · 2006 to 2020
$23.3M
CELLULAR CHANGES ALTERING SYNAPTIC CONNECTIVITY IN PRECLINICAL ADR01AG042475 · NIA · UNIVERSITY OF KENTUCKY · PI NELSON, PETER T. · 2013 to 2017
$1.5M
Involvement of myelin integrity in Alzheimer's disease pathogenesisK99AG044445 · NIA · UNIVERSITY OF KENTUCKY · PI BACHSTETTER, ADAM D · 2014 to 2015
$175k
NCI NIH HHS P30 CA177558NIA NIH HHS K99 AG044445NIA NIH HHS P30 AG028383NIA NIH HHS R01 AG042475
6 · The paper itself

Abstract

introductionNeuropathological, genetic, and biochemical studies have provided support for the hypothesis that microglia participate in Alzheimer's disease (AD) pathogenesis. Despite the extensive characterization of AD microglia, there are still many unanswered questions, and little is known about microglial morphology in other common forms of age-related dementia: particularly, dementia with Lewy bodies (DLB) and hippocampal sclerosis of aging (HS-Aging). In addition, no prior studies have attempted to compare and contrast the microglia morphology in the hippocampus of various neurodegenerative conditions.

resultsHere we studied cases with pathologically-confirmed AD (n = 7), HS-Aging (n = 7), AD + HS-aging (n = 4), DLB (n = 12), and normal (cognitively intact) controls (NC) (n = 9) from the University of Kentucky Alzheimer's Disease Center autopsy cohort. We defined five microglia morphological phenotypes in the autopsy samples: ramified, hypertrophic, dystrophic, rod-shaped, and amoeboid. The Aperio ScanScope digital neuropathological tool was used along with two well-known microglial markers: IBA1 (a marker for both resting and activated microglia) and CD68 (a lysosomal marker in macrophages/microglia associated with phagocytic cells). Hippocampal staining analyses included studies of subregions within the hippocampal formation and nearby white matter. Using these tools and methods, we describe variation in microglial characteristics that show some degree of disease specificity, including, (1) increased microglia density and number in HS-aging and AD + HS-aging; (2) low microglia density in DLB; (3) increased number of dystrophic microglia in HS-aging; and (4) increased proportion of dystrophic to all microglia in DLB.

conclusionsWe conclude that variations in morphologies among microglial cells, and cells of macrophage lineage, can help guide future work connecting neuroinflammatory mechanisms with specific neurodegenerative disease subtypes.

Indexed as

AgedAged, 80 and overAgingAlzheimer DiseaseAntigens, CDAntigens, Differentiation, MyelomonocyticAutopsyCalcium-Binding ProteinsCD68 MoleculeDementiaDNA-Binding ProteinsFemaleHippocampusHumansLewy Body DiseaseMaleAIF1 protein, humanAntigens, CDAntigens, Differentiation, MyelomonocyticCalcium-Binding ProteinsCD68 antigen, humanCD68 MoleculeDNA-Binding ProteinsMicrofilament Proteins

Identifiers

PMID26001591
PMCPMC4489160
OpenAlexW2138650666

What OpenQuestion holds

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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.