Evidence map›Paper›PMID 37731949›Full record

ArticlePNAS nexus2023

Severe acute respiratory syndrome coronavirus 2 infection leads to Tau pathological signature in neurons.

Cristina Di Primio, Paola Quaranta, Marianna Mignanelli, Giacomo Siano, Matteo Bimbati, Arianna Scarlatti, Carmen Rita Piazza, Piero Giorgio Spezia, Paola Perrera, Fulvio Basolo and 4 more

Abstract read
In one paragraph

Article in PNAS nexus, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Review
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  14. The Functional Consequences of Long COVID Need to Be Addressed by Occupational Therapists.The American journal of occupational therapy : official publication of the American Occupational Therapy 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

14 authors.

Cristina Di PrimioInstitute of Neuroscience, Italian National Research Council (CNR), Pisa 56124, Italy.ORCID https://orcid.org/0000-0003-2140-3696
Paola QuarantaInstitute of Neuroscience, Italian National Research Council (CNR), Pisa 56124, Italy.ORCID https://orcid.org/0000-0001-8828-0905
Marianna MignanelliLaboratorio di Biologia Bio@SNS, Scuola Normale Superiore di Pisa, Pisa 56126, Italy.
Giacomo SianoLaboratorio di Biologia Bio@SNS, Scuola Normale Superiore di Pisa, Pisa 56126, Italy.ORCID https://orcid.org/0000-0003-4320-5631
Matteo BimbatiLaboratorio di Biologia Bio@SNS, Scuola Normale Superiore di Pisa, Pisa 56126, Italy.
Arianna ScarlattiLaboratorio di Biologia Bio@SNS, Scuola Normale Superiore di Pisa, Pisa 56126, Italy.
Carmen Rita PiazzaRetrovirus Center, Virology Section, Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa 56100, Italy.
Piero Giorgio SpeziaRetrovirus Center, Virology Section, Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa 56100, Italy.
Paola PerreraRetrovirus Center, Virology Section, Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa 56100, Italy.
Fulvio BasoloDepartment of Surgical, Medical and Molecular Pathology, University Hospital of Pisa, Pisa 56124, Italy.ORCID https://orcid.org/0000-0003-1657-5020
Anello Marcello PomaDepartment of Surgical, Medical and Molecular Pathology, University Hospital of Pisa, Pisa 56124, Italy.ORCID https://orcid.org/0000-0002-0212-8249
Mario CostaInstitute of Neuroscience, Italian National Research Council (CNR), Pisa 56124, Italy.
Mauro PistelloRetrovirus Center, Virology Section, Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa 56100, Italy.ORCID https://orcid.org/0000-0003-0908-6253
Antonino CattaneoLaboratorio di Biologia Bio@SNS, Scuola Normale Superiore di Pisa, Pisa 56126, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

COVID-19 has represented an issue for global health since its outbreak in March 2020. It is now evident that the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection results in a wide range of long-term neurological symptoms and is worryingly associated with the aggravation of Alzheimer's disease. Little is known about the molecular basis of these manifestations. Here, several strain variants were used to infect SH-SY5Y neuroblastoma cells and K18-hACE C57BL/6J mice. The Tau phosphorylation profile and aggregation propensity upon infection were investigated on cellular extracts, subcellular fractions, and brain tissue. The viral proteins spike, nucleocapsid, and membrane were overexpressed in SH-SY5Y cells, and the direct interaction and effect on Tau phosphorylation were checked using immunoblot experiments. Upon infection, Tau is phosphorylated at several pathological epitopes associated with Alzheimer's disease and other tauopathies. Moreover, this event increases Tau's propensity to form insoluble aggregates and alters its subcellular localization. Our data support the hypothesis that SARS-CoV-2 infection in the central nervous system triggers downstream effects altering Tau function, eventually leading to the impairment of neuronal function.

Indexed as

COVID-19neuro-COVIDphospho-TauSARS-CoV-2Tau

Identifiers

PMID37731949
PMCPMC10508204

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.