Molecular biomarkers of epileptogenesis
Abstract
The heterogeneity of epilepsy syndromes and pathologies creates a great challenge for the search for biomarkers. Not surprisingly, identification of a marker that is specific and sensitive for a given epileptogenic pathology remains an unmet need. There have, however, been several studies of major epileptogenic etiologies like traumatic brain injury that aimed to identify molecular markers in blood and cerebrospinal fluid that predict outcome, by using proteomics and metabolomics. Unfortunately, epileptogenesis has not been analyzed as an outcome measure. Another question to be explored is whether a palette of molecular markers is needed, rather than a single molecule, with each marker probing a different component of epileptogenic pathology. Further, perhaps multiple biomarker platforms (e.g., imaging, proteomics, electrophysiology) should be used in combination and/or in a defined temporal sequence.
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Limbic epileptogenesis involves a partially-understood molecular cascade that results in aberrant neuronal connectivity and chronic recurrent spontaneous seizures.
“Development of TLE or limbic epileptogenesis [4, 5] involves a partially-understood molecular cascade [6] that results in aberrant neuronal connectivity [7, 8] from a multi-architecture neuronal network of the limbic system connected to hippocampal formation [9] that contributes to a systemic process in the brain that leads to chronic recurrent spontaneous seizures [10].”
From Hippocampal neuro-networks and dendritic spine perturbations in epileptogenesis are attenuated by neuroprotectin D1 (2015) · cites this paper as [6]
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- Authors
- Pitkänen, A., & Lukasiuk, K.
- Affiliations
- University of Eastern Finland (FI)
- The Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland
- ORCID
- Pitkänen, Asla
- Venue
- Biomarkers in Medicine
- Publisher
- Informa UK Limited
- Published
- 2011-10
- Volume
- 5
- Issue
- 5
- Pages
- 629-633
- ISSN
- 1752-0363 (ISSN-L)
- 1752-0371
- OpenAlex
- W2003470910
- Cited by
- 40
- References
- 51
- Citations by year
- 2026: 1 · 2025: 3 · 2023: 2 · 2022: 1 · 2020: 3 · 2019: 1 · 2017: 8 · 2016: 6 · 2015: 6 · 2014: 3 · 2013: 3 · 2012: 2
- FWCI
- 1.97
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biomarkers in Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- statutory funds of the Nencki Institute
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolomics and Mass Spectrometry Studies
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- epileptogenesis, molecular biomarkers, epilepsy, traumatic brain injury, cerebrospinal fluid, blood biomarkers, proteomics, metabolomics, biomarker panel, outcome prediction
- MeSH terms
- Brain Injuries, Humans, Biomarkers, MicroRNAs, Proteomics, Metabolomics, Transcriptome
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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