Evidence map›Paper›PMID 41631069›Full record

ArticleCureus2026

TrkB Overexpression via Gene Therapy: Enhanced Optic Nerve Uptake With Associated Increases in Mitochondria and Axoplasmic Transport.

Sadat Yazdouni, Andrew Osborne, Keith R Martin

Abstract read
In one paragraph

Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

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

3 authors.

Sadat YazdouniSchool of Clinical Medicine, University of Cambridge, Cambridge, GBR.
Andrew OsborneJohn van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge, GBR.
Keith R MartinDepartment of Ophthalmology, Centre for Eye Research Australia, Melbourne, AUS.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionGlaucoma is a progressive neurodegenerative disease that affects retinal ganglion cells (RGCs), ultimately leading to vision loss. In this study, we investigated gene therapy-mediated transduction of RGCs and examined axonal transport changes in the optic nerve using a viral vector designed to upregulate tropomyosin receptor kinase B (TrkB) expression.

methodTrkB expression was evaluated in retinae and optic nerves of rats following genetic intravitreal delivery of AAV2-TrkB. Axonal transport and preliminary mitochondrial changes were assessed in optic nerves by immunohistochemical staining for kinesin and voltage-dependent anion channel (VDAC), a mitochondrial component.

resultsThe results revealed an approximately 30% increase in TrkB expression in the retina, which was confirmed to be vector-driven by a P2A tag attached to the TrkB protein. This increased protein expression could be seen independent of injury and in eyes with elevated intraocular pressure. Observations along the optic nerve of rats treated with AAV2-TrkB revealed elevated transport of TrkB along axons (50% in TrkB, 120% in P2A tag) and significant increases in kinesin (12%) and VDAC (16%) immunoreactivity.

conclusionThis study provides early indications that improving TrkB expression in the eye may increase anterograde transport of motor proteins, which in turn could improve mitochondrial transport within the optic nerve.

Indexed as

adeno-associated viral vectoraxoplasmic transportbrain-derived neurotrophic factor (bdnf)glaucomaocular gene therapyrodent modeltropomyosin-related receptor kinase-b

Identifiers

PMID41631069
PMCPMC12860902

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