Evidence map›Paper›PMID 18700006›Full record

ArticleBMC neuroscience2008

Detailed immunohistochemical characterization of temporal and spatial progression of Alzheimer's disease-related pathologies in male triple-transgenic mice.

Michael A Mastrangelo, William J Bowers

Open access · goldAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 4% 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

116 citing papers in PubMed, 1 synthesis or guideline pooled it, 247 citations in OpenAlex.

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  19. The lateral entorhinal cortex is a hub for local and global dysfunction in early Alzheimer's disease states.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022
    Article
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56 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 1 institution in 1 country.

Michael A MastrangeloDepartment of Neurology, University of Rochester Medical Center, Rochester, NY 14642, USA. michael_mastrangelo@urmc.rochester.edu
William J Bowers
University of Rochester Medical Center · US

Funding

Gene-based TNF-alpha activity modulation in 3xTg-AD miceR01AG026328 · NIA · UNIVERSITY OF ROCHESTER · PI BOWERS, WILLIAM J. · 2007 to 2011
$1.4M
Novel Mouse Model to Dissect Alzheimer's Disease PathophysiologyR01AG023593 · NIA · UNIVERSITY OF ROCHESTER · PI BOWERS, WILLIAM J. · 2004 to 2008
$1.3M
NIA NIH HHS R01 AG023593NIA NIH HHS R01-AG023593NIA NIH HHS R01 AG026328NIA NIH HHS R01-AG026328
6 · The paper itself

Abstract

backgroundSeveral transgenic animal models genetically predisposed to develop Alzheimer's disease (AD)-like pathology have been engineered to facilitate the study of disease pathophysiology and the vetting of potential disease-modifying therapeutics. The triple transgenic mouse model of AD (3xTg-AD) harbors three AD-related genetic loci: human PS1M146V, human APPswe, and human tauP301L. These mice develop both amyloid plaques and neurofibrillary tangle-like pathology in a progressive and age-dependent manner, while these pathological hallmarks are predominantly restricted to the hippocampus, amygdala, and the cerebral cortex the main foci of AD neuropathology in humans. This model represents, at present, one of the most advanced preclinical tools available and is being employed ever increasingly in the study of mechanisms underlying AD, yet a detailed regional and temporal assessment of the subtleties of disease-related pathologies has not been reported. METHODS AND

resultsIn this study, we immunohistochemically documented the evolution of AD-related transgene expression, amyloid deposition, tau phosphorylation, astrogliosis, and microglial activation throughout the hippocampus, entorhinal cortex, primary motor cortex, and amygdala over a 26-month period in male 3xTg-AD mice. Intracellular amyloid-beta accumulation is detectable the earliest of AD-related pathologies, followed temporally by phospho-tau, extracellular amyloid-beta, and finally paired helical filament pathology. Pathology appears to be most severe in medial and caudal hippocampus. While astrocytic staining remains relatively constant at all ages and regions assessed, microglial activation appears to progressively increase temporally, especially within the hippocampal formation.

conclusionThese data fulfill an unmet need in the ever-widening community of investigators studying 3xTg-AD mice and provide a foundation upon which to design future experiments that seek to examine stage-specific disease mechanisms and/or novel therapeutic interventions for AD.

Indexed as

Disease Models, AnimalAge FactorsAlzheimer DiseaseAnimalsBrainBrain ChemistryDisease ProgressionHumansImmunohistochemistryMaleMiceMice, TransgenicNeurofibrillary TanglesPlaque, Amyloid

Identifiers

PMID18700006
PMCPMC2527610
OpenAlexW2136466563

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.