Evidence map›Paper›PMID 42079190›Full record

ArticlebioRxiv : the preprint server for biology2026

Intranasal CRISPR-lipid nanoparticles targeting MAPK9 reduce neuroinflammation after traumatic brain injury.

Goknur Kara, Yaqoob Ali, Jessica López-Espinosa, Peter Park, Morgan Holcomb, Hannah Flinn, Noah Taylor, Tyler Galbraith, Fransisca Leonard, Sonia Villapol

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Goknur KaraDepartment of Neurosurgery and Center for Neuroregeneration, Houston Methodist Research Institute, Houston, TX, USA.ORCID 0000-0002-5905-9758
Yaqoob AliDepartment of Neurology, Houston Methodist Research Institute, Houston, TX, USA.
Jessica López-EspinosaDepartment of Neurosurgery and Center for Neuroregeneration, Houston Methodist Research Institute, Houston, TX, USA.
Peter ParkDepartment of Neurosurgery and Center for Neuroregeneration, Houston Methodist Research Institute, Houston, TX, USA.
Morgan HolcombDepartment of Neurosurgery and Center for Neuroregeneration, Houston Methodist Research Institute, Houston, TX, USA.
Hannah FlinnDepartment of Neurosurgery and Center for Neuroregeneration, Houston Methodist Research Institute, Houston, TX, USA.
Noah TaylorDepartment of Neurosurgery and Center for Neuroregeneration, Houston Methodist Research Institute, Houston, TX, USA.
Tyler GalbraithDepartment of Nanomedicine, Houston Methodist Research Institute, Houston, TX, USA.
Fransisca LeonardDepartment of Transplant Oncology, Houston Methodist Research Institute, Houston, TX, USA.
Sonia VillapolDepartment of Neurosurgery and Center for Neuroregeneration, Houston Methodist Research Institute, Houston, TX, USA.ORCID 0000-0002-6174-4113

Funding

Microbiota-targeted approaches to resolve dysbiosis-induced AD neuropathology following brain injury.R56AG080920 · NIA · METHODIST HOSPITAL RESEARCH INSTITUTE · PI VILLAPOL, SONIA · 2023 to 2024
$1.3M
Intranasal Delivery of Telomerase Reverse Transcriptase mRNA for Therapy ofTraumatic Brain InjuryR21NS127265 · NINDS · METHODIST HOSPITAL RESEARCH INSTITUTE · PI GODIN, BIANA, VILLAPOL, SONIA · 2022 to 2022
$444k
The role of the gut microbiome in the neuropathology of traumatic brain injuryR21NS106640 · NINDS · METHODIST HOSPITAL RESEARCH INSTITUTE · PI VILLAPOL, SONIA · 2018 to 2019
$431k
NIA NIH HHS R56 AG080920NINDS NIH HHS R21 NS106640NINDS NIH HHS R21 NS127265
6 · The paper itself

Abstract

Traumatic brain injury (TBI) triggers a sustained neuroinflammatory response driven by activated microglia, which contributes to secondary injury and long-term neurological dysfunction. Therapeutic reprogramming of microglial activation from a pro-inflammatory (M1-like) to a reparative (M2-like) phenotype represents a promising strategy; however, the lack of cell-specific targeting within an injured brain has limited clinical translation. Here, we developed a targeted gene-editing nanotherapy to modulate post-traumatic innate immune responses. Lipid nanoparticles (LNPs) encapsulating CRISPR-Cas12a components were engineered to target mitogen-activated protein kinase-9 (MAPK9), a key regulator of pro-inflammatory signaling, and were conjugated with an Iba-1 antibody (Iba-1-CRISPR-LNPs) to enable selective targeting of microglia.

Indexed as

brain traumaCRISPRlipid nanoparticlesMAPK9microglia reprogrammingneuroinflammation

Identifiers

PMID42079190
PMCPMC13131497

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.