Evidence map›Paper›PMID 34655981›Full record

ArticleNeurobiology of aging2022

Pathological tau and reactive astrogliosis are associated with distinct functional deficits in a mouse model of tauopathy.

Henika Patel, Pablo Martinez, Abigail Perkins, Xavier Taylor, Nur Jury, David McKinzie, Cristian A Lasagna-Reeves

Open access · hybridAbstract read
In one paragraph

Article in Neurobiology of aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

30 citing papers in PubMed, 66 citations in OpenAlex.

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  13. Tau depletion diminishes vascular amyloid-related deficits in a mouse model of cerebral amyloid angiopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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  19. Inpp5d haplodeficiency alleviates tau pathology in the PS19 mouse model of Tauopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
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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 1 institution in 1 country.

Henika PatelStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA; Department of Anatomy, Cell Biology & Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
Pablo MartinezStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA; Department of Anatomy, Cell Biology & Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
Abigail PerkinsStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA; Department of Anatomy, Cell Biology & Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
Xavier TaylorStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA; Department of Anatomy, Cell Biology & Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
Nur JuryStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA; Department of Anatomy, Cell Biology & Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
David McKinzieStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA; Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, USA.
Cristian A Lasagna-ReevesStark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA; Department of Anatomy, Cell Biology & Physiology, Indiana University School of Medicine, Indianapolis, IN, USA; Center for Computational Biology and Bioinformatics, Indiana University School of Medicine, Indianapolis, IN, USA. Electronic address: clasagna@iu.edu.
Indiana University School of Medicine

Funding

Tau-seed protein interactome and its role in neurodegenerative tauopathiesR01NS119280 · NINDS · INDIANA UNIVERSITY INDIANAPOLIS · PI LASAGNA-REEVES, CRISTIAN · 2020 to 2024
$3.5M
Comprehensive identification and validation of immune and inflammatory signatures associated to Cerebral Amyloid Angiopathy (CAA) utilizing the NanoString technology.R01AG059639 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LASAGNA-REEVES, CRISTIAN · 2018 to 2022
$3.1M
Studying the Physiological Role of Nuak1 in Tau PathogenesisK22NS092688 · NINDS · INDIANA UNIVERSITY INDIANAPOLIS · PI LASAGNA-REEVES, CRISTIAN · 2015 to 2019
$938k
NIA NIH HHS R01 AG059639NINDS NIH HHS K22 NS092688NINDS NIH HHS R01 NS119280
6 · The paper itself

Abstract

Pathological aggregation of tau and neuroinflammatory changes mark the clinical course of Alzheimer's disease and related tauopathies. To understand the correlation between these pathological hallmarks and functional deficits, we assessed behavioral and physiological deficits in the PS19 mouse model, a broadly utilized model of tauopathy. At 9 months, PS19 mice have characteristic hyperactive behavior, a decline in motor strength, and deterioration in physiological conditions marked by lower body temperature, reduced body weight, and an increase in measures of frailty. Correlation of these deficits with different pathological hallmarks revealed that pathological tau species, characterized by soluble p-tau species, and tau seeding bioactivity correlated with impairment in grip strength and thermal regulation. On the other hand, astrocyte reactivity showed a positive correlation with the hyperactive behavior of the PS19 mice. These results suggest that a diverse spectrum of soluble pathological tau species could be responsible for different symptoms and that neuroinflammation could contribute to functional deficits independently from tau pathology. These observations enhance the necessity of a multi-targeted approach for the treatment of neurodegenerative tauopathies.

Indexed as

AnimalsBehavior, AnimalBody Temperature RegulationDisease Models, AnimalFemaleFrailtyGliosisHand StrengthHumansMaleMice, TransgenicMotor ActivityNeuroinflammatory DiseasesProtein Aggregation, PathologicalTauopathiestau Proteinstau ProteinsBehaviorGliosisTauopathy modelTau pathology

Identifiers

PMID34655981
PMCPMC8671336
OpenAlexW3201487388

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.