Evidence map›Paper›PMID 31531390›Full record

ArticleNPJ Parkinson's disease2019

Infection with mosquito-borne alphavirus induces selective loss of dopaminergic neurons, neuroinflammation and widespread protein aggregation.

Collin M Bantle, Aaron T Phillips, Richard J Smeyne, Savannah M Rocha, Ken E Olson, Ronald B Tjalkens

Open access · goldAbstract read
In one paragraph

Article in NPJ Parkinson's disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
11.1field-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

67 citing papers in PubMed, 89 citations in OpenAlex.

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7 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

6 authors at 2 institutions in 1 country.

Collin M Bantle1Department of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, CO 80523 USA.
Aaron T Phillips1Department of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, CO 80523 USA.
Richard J Smeyne3Department of Neuroscience, Vickie & Jack Farber Institute for Neuroscience, Thomas Jefferson University, Philadelphia, PA 19107 USA.
Savannah M Rocha2Arthropod-Borne and Infectious Disease Laboratory, Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO 80523 USA.
Ken E Olson2Arthropod-Borne and Infectious Disease Laboratory, Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO 80523 USA.
Ronald B Tjalkens1Department of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, CO 80523 USA.
Colorado State University · USJefferson Hospital for Neuroscience · US

Funding

Encephalitic viral infection and susceptibility to dopaminergic neurotoxinsR01ES030937 · NIEHS · COLORADO STATE UNIVERSITY · PI TJALKENS, RONALD · 2019 to 2021
$1.9M
NIEHS NIH HHS R01 ES030937
6 · The paper itself

Abstract

Neuroinvasive infections with mosquito-borne alphaviruses such as Western equine encephalitis virus (WEEV) can cause post-encephalitic parkinsonism. To understand the mechanisms underlying these neurological effects, we examined the capacity of WEEV to induce progressive neurodegeneration in outbred CD-1 mice following non-lethal encephalitic infection. Animals were experientally infected with recombinant WEEV expressing firefly luciferase or dsRed (RFP) reporters and the extent of viral replication was controlled using passive immunotherapy. WEEV spread along the neuronal axis from the olfactory bulb to the entorhinal cortex, hippocampus and basal midbrain by 4 days post infection (DPI). Infection caused activation of microglia and astrocytes, selective loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and neurobehavioral abnormalities. After 8 weeks, surviving mice displayed continued loss of dopamine neurons in the SNpc, lingering glial cell activation and gene expression profiles consistent with a neurodegenerative phenotype. Strikingly, prominent proteinase K-resistant protein aggregates were present in the the entorhinal cortex, hippocampus and basal midbrain that stained positively for phospho-serine129 α-synuclein (SNCA). These results indicate that WEEV may cause lasting neurological deficits through a severe neuroinflammatory response promoting both neuronal injury and protein aggregation in surviving individuals.

Indexed as

NeuroimmunologyParkinson's disease

Identifiers

PMID31531390
PMCPMC6744428
OpenAlexW2972589620

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.