Evidence map›Paper›PMID 30488653›Full record

ArticleAging cell2019

Temporal and regional progression of Alzheimer's disease-like pathology in 3xTg-AD mice.

Ramona Belfiore, Alexis Rodin, Eric Ferreira, Ramon Velazquez, Caterina Branca, Antonella Caccamo, Salvatore Oddo

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 208 papers.

0numbers the graph read from it
0cells of the map it votes in
208citing papers in PubMed
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

208 citing papers in PubMed, 333 citations in OpenAlex.

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  17. Alzheimer's Pathology Enhances Excitatory Synaptic Input and Integration in VTA Dopamine Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
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148 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

7 authors at 2 institutions in 2 countries.

Ramona BelfioreThe Arizona State University-Banner Neurodegenerative Disease Research Center at the Biodesign Institute, Arizona State University, Tempe, Arizona.
Alexis RodinThe Arizona State University-Banner Neurodegenerative Disease Research Center at the Biodesign Institute, Arizona State University, Tempe, Arizona.
Eric FerreiraThe Arizona State University-Banner Neurodegenerative Disease Research Center at the Biodesign Institute, Arizona State University, Tempe, Arizona.
Ramon VelazquezThe Arizona State University-Banner Neurodegenerative Disease Research Center at the Biodesign Institute, Arizona State University, Tempe, Arizona.
Caterina BrancaThe Arizona State University-Banner Neurodegenerative Disease Research Center at the Biodesign Institute, Arizona State University, Tempe, Arizona.
Antonella CaccamoThe Arizona State University-Banner Neurodegenerative Disease Research Center at the Biodesign Institute, Arizona State University, Tempe, Arizona.
Salvatore OddoThe Arizona State University-Banner Neurodegenerative Disease Research Center at the Biodesign Institute, Arizona State University, Tempe, Arizona.ORCID 0000-0001-7304-7430
Arizona State University · USUniversity of Catania · IT

Funding

Molecular interplay between Aβ, tau and mTOR: Mechanisms of neurodegenerationRF1AG037637 · NIA · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · PI ODDO, SALVATORE · 2016 to 2016
$1.1M
NIA NIH HHS RF1 AG037637
6 · The paper itself

Abstract

Accumulation of amyloid-β (Aβ) and fibrillary tangles, as well as neuroinflammation and memory loss, are hallmarks of Alzheimer's disease (AD). After almost 15 years from their generation, 3xTg-AD mice are still one of the most used transgenic models of AD. Converging evidence indicates that the phenotype of 3xTg-AD mice has shifted over the years and contradicting reports about onset of pathology or cognitive deficits are apparent in the literature. Here, we assessed Aβ and tau load, neuroinflammation, and cognitive changes in 2-, 6-, 12-, and 20-month-old female 3xTg-AD and nontransgenic (NonTg) mice. We found that ~80% of the mice analyzed had Aβ plaques in the caudal hippocampus at 6 months of age, while 100% of them had Aβ plaques in the hippocampus at 12 months of age. Cortical Aβ plaques were first detected at 12 months of age, including in the entorhinal cortex. Phosphorylated Tau at Ser202/Thr205 and Ser422 was apparent in the hippocampus of 100% of 6-month-old mice, while only 50% of mice showed tau phosphorylation at Thr212/Ser214 at this age. Neuroinflammation was first evident in 6-month-old mice and increased as a function of age. These neuropathological changes were clearly associated with progressive cognitive decline, which was first apparent at 6 months of age and became significantly worse as the mice aged. These data indicate a consistent and predictable progression of the AD-like pathology in female 3xTg-AD mice, and will facilitate the design of future studies using these mice.

Indexed as

Disease ProgressionAgingAlzheimer DiseaseAmyloid beta-PeptidesAnimalsGliosisHippocampusMemory DisordersMice, Inbred C57BLMice, TransgenicMicrogliaPhosphorylationPlaque, Amyloidtau ProteinsTime FactorsAmyloid beta-Peptidestau ProteinsAPPAβcognitive deficitsinflammationmicroglianeuroinflammationplaquestanglestautransgenic mice

Identifiers

PMID30488653
PMCPMC6351836
OpenAlexW2902887888

What Socratic holds

Textmetadata
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 Socratic graph.