Evidence map›Paper›PMID 39767775›Full record

ArticleBiomedicines2024

Mossy Fiber Sprouting in Temporal Lobe Epilepsy: The Impact of Netrin-1, DCC, and Gene Expression Changes.

Melis Onay, Patrick N Harter, Katherina Weber, Albrecht Piiper, Marcus Czabanka, Karl H Plate, Thomas M Freiman, Florian Gessler, Barbara Puhahn-Schmeiser

Abstract read
In one paragraph

Article in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

9 authors.

Melis OnayDepartment of Internal Medicine I, Goethe University, Theodor-Stern-Kai 7, 60596 Frankfurt am Main, Germany.
Patrick N HarterDepartment of Neuropathology, Ludwig-Maximillians-University Munich, Feodor-Lynen-Str. 23, 81377 Munich, Germany.
Katherina WeberDepartment of Neuropathology (Edinger Institute), Goethe University, Heinrich-Hoffmann-Straße 7, 60528 Frankfurt am Main, Germany.
Albrecht PiiperDepartment of Internal Medicine I, Goethe University, Theodor-Stern-Kai 7, 60596 Frankfurt am Main, Germany.
Marcus CzabankaDepartment of Neurosurgery, Goethe University, Schleusenweg 16, 60528 Frankfurt am Main, Germany.
Karl H PlateDepartment of Neuropathology (Edinger Institute), Goethe University, Heinrich-Hoffmann-Straße 7, 60528 Frankfurt am Main, Germany.
Thomas M FreimanDepartment of Neurosurgery, Rostock University Medical Center, Schilingallee 35, 18057 Rostock, Germany.ORCID 0000-0002-2591-2829
Florian GesslerDepartment of Neurosurgery, Rostock University Medical Center, Schilingallee 35, 18057 Rostock, Germany.ORCID 0000-0002-3471-0575
Barbara Puhahn-SchmeiserDepartment of Neurosurgery, Freiburg University Medical Center, Breisacher Str. 64, 79106 Freiburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTemporal lobe epilepsy (TLE) is the most common form of drug-resistant epilepsy, often associated with hippocampal sclerosis (HS), which involves selective neuronal loss in the Cornu Ammonis subregion 1 CA1 and CA4 regions of the hippocampus. Granule cells show migration and mossy fiber sprouting, though the mechanisms remain unclear. Microglia play a role in neurogenesis and synaptic modulation, suggesting they may contribute to epilepsy. This study examines the role of microglia and axonal guidance molecules in neuronal reorganization in TLE.

methodsNineteen hippocampal samples from patients with TLE undergoing epilepsy surgery were analyzed. Microglial activity (M1/M2-like microglia) and neuronal guidance molecules were assessed using microscopy and semi-automated techniques. Gene expression was evaluated using the nCounter Expression Profiling method.

resultsNeuronal cell loss was correlated with decreased activity of the M1 microglial phenotype. In the CA2 region, neuronal preservation was linked to increased mossy fiber sprouting and microglial presence. Neuronal markers such as Deleted in Colorectal Cancer (DCC) and Synaptopodin were reduced in areas of cell death, while Netrin-1 was elevated in the granule cell layer, potentially influencing mossy fiber sprouting. The nCounter analysis revealed downregulation of genes involved in neuronal activity (e.g., NPAS4, BCL-2, GRIA1) and upregulation of IκB, indicating reduced neuroinflammation.

conclusionsThis study suggests reduced neuroinflammation in areas of neuronal loss, while regions with preserved neurons showed mossy fiber sprouting associated with microglia, Netrin-1, and DCC.

Indexed as

DCChippocampal sclerosisIκBαM1 phenotypeM2 phenotypemicrogliaNetrin-1synaptopodintemporal lobe epilepsy

Identifiers

PMID39767775
PMCPMC11672915

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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.