Evidence map›Paper›PMID 35361832›Full record

ArticleScientific reports2022

SARS-CoV-2 spike protein induces cognitive deficit and anxiety-like behavior in mouse via non-cell autonomous hippocampal neuronal death.

Junyoung Oh, Woo-Hyun Cho, Ellane Barcelon, Kwang Hwan Kim, Jinpyo Hong, Sung Joong Lee

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

37 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
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  6. Neuroimmune pathophysiology of long COVID.Psychiatry and clinical neurosciences · 2025
    Review
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  19. Infectious Diseases.Advances in neurobiology · 2024
    Review
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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

6 authors at 1 institution in 1 country.

Junyoung Oh *Department of Neuroscience and Physiology, Dental Research Institute, School of Dentistry, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, Republic of Korea.
Woo-Hyun Cho *Department of Neuroscience and Physiology, Dental Research Institute, School of Dentistry, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, Republic of Korea.
Ellane BarcelonDepartment of Neuroscience and Physiology, Dental Research Institute, School of Dentistry, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, Republic of Korea.
Kwang Hwan KimDepartment of Brain and Cognitive Sciences, College of Natural Sciences and School of Dentistry, Seoul National University, Seoul, 08826, Republic of Korea.
Jinpyo HongOATC Research Center for Neurodiseases, Seoul, 08833, Republic of Korea.
Sung Joong LeeDepartment of Neuroscience and Physiology, Dental Research Institute, School of Dentistry, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, Republic of Korea. sjlee87@snu.ac.kr.
Seoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is accompanied by chronic neurological sequelae such as cognitive decline and mood disorder, but the underlying mechanisms have not yet been elucidated. We explored the possibility that the brain-infiltrating SARS-CoV-2 spike protein contributes to the development of neurological symptoms observed in COVID-19 patients in this study. Our behavioral study showed that administration of SARS-CoV-2 spike protein S1 subunit (S1 protein) to mouse hippocampus induced cognitive deficit and anxiety-like behavior in vivo. These neurological symptoms were accompanied by neuronal cell death in the dorsal and ventral hippocampus as well as glial cell activation. Interestingly, the S1 protein did not directly induce hippocampal cell death in vitro. Rather, it exerted neurotoxicity via glial cell activation, partially through interleukin-1β induction. In conclusion, our data suggest a novel pathogenic mechanism for the COVID-19-associated neurological symptoms that involves glia activation and non-cell autonomous hippocampal neuronal death by the brain-infiltrating S1 protein.

Indexed as

Cognitive DysfunctionCOVID-19AnimalsAntibodies, ViralAnxietyCell DeathCognitionHippocampusHumansMembrane GlycoproteinsMiceSARS-CoV-2Spike Glycoprotein, CoronavirusViral Envelope ProteinsAntibodies, ViralMembrane GlycoproteinsSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2Viral Envelope Proteins

Identifiers

PMID35361832
PMCPMC8970073
OpenAlexW4226054687

What OpenQuestion 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 OpenQuestion graph.