Evidence map›Paper›PMID 36970910›Full record

ArticleJournal of Alzheimer's disease : JAD2023

Influence of Host Age on Intracranial AAV9 TauP301L Induced Tauopathy.

Amber M Tetlow, Brianna M Jackman, Mohammed M Alhadidy, Varshini Perumal, David G Morgan, Marcia N Gordon

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

Article in Journal of Alzheimer's disease : JAD, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 51% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

6 authors at 1 institution in 1 country.

Amber M TetlowDepartment of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA.
Brianna M JackmanDepartment of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA.
Mohammed M AlhadidyDepartment of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA.
Varshini PerumalDepartment of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA.
David G MorganDepartment of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA.
Marcia N GordonDepartment of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA.
Michigan State University · US

Funding

Influence of systemic immune inflammation upon the tauopathy phenotype in mouse modelsR01AG051500 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI MORGAN, DAVID · 2016 to 2020
$3.5M
Geroscience approaches to mitigate tauopathy in aged mouse brainR01AG062217 · NIA · MICHIGAN STATE UNIVERSITY · PI GORDON, MARCIA N · 2018 to 2022
$3.0M
NIA NIH HHS R01 AG051500NIA NIH HHS R01 AG062217
6 · The paper itself

Abstract

backgroundAdvanced age is the greatest risk factor for the development of Alzheimer's disease (AD). This implies that some aspect of the aged milieu is possibly accelerating the development of AD related pathologies.

objectiveWe hypothesized that intracranially injected with AAV9 tauP301L may cause a greater degree of pathology in old versus young mice.

methodsAnimals were injected with viral vectors overexpressing the mutant tauP301L or control protein (green fluorescent protein, GFP) into the brains of mature, middle-aged, and old C57BL/6Nia mice. The tauopathy phenotype was monitored four months after injection using behavioral, histological, and neurochemical measures.

resultsPhosphorylated-tau immunostaining (AT8) or Gallyas staining of aggregated tau increased with age, but other measures of tau accumulation were not significantly affected. Overall, AAV-tau injected mice had impaired radial arm water maze performance, increased microglial activation, and showed evidence of hippocampal atrophy. Aging impaired open field and rotarod performance in both AAV-tau and control mice. The efficiency of viral transduction and gene expression were the same at all animal ages.

conclusionWe conclude that tauP301L over expression results in a tauopathy phenotype with memory impairment and accumulation of aggregated tau. However, the effects of aging on this phenotype are modest and not detected by some markers of tau accumulation, similar to prior work on this topic. Thus, although age does influence the development of tauopathy, it is likely that other factors, such as ability to compensate for tau pathology, are more responsible for the increased risk of AD with advanced age.

Indexed as

Alzheimer DiseaseTauopathiesAnimalsBrainDisease Models, AnimalGreen Fluorescent ProteinsMiceMice, Inbred C57BLMice, Transgenictau ProteinsGreen Fluorescent Proteinstau ProteinsAdeno-associated virusaginganimal disease modelstauopathy

Identifiers

PMID36970910
PMCPMC10540220
OpenAlexW4360841940

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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.