ReviewCurrent neurology and neuroscience reports2025
Pathophysiological Mechanisms Fostering Developmental and Epileptic Encephalopathies (DEE): a Complex Interplay between Genetics, Inflammation and Neurodegeneration.
Review in Current neurology and neuroscience reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of the reviewPreclinical and clinical evidence support the notion that in Developmental and Epileptic Encephalopathies (DEEs) both neurodevelopmental and progressive alterations coexist. Several studies have contributed to the identification of pathophysiological mechanisms underlying DEEs, allowing novel interpretative meanings regarding the mechanisms involved in the progression of DEE symptomatology. The purpose of this review is to critically discuss emerging evidence linking DEEs, genetics, inflammation, and neurodegeneration. RECENT
findingsIn the last two decades, genetic findings have highlighted the role of cellular processes involved in both early neurodevelopment and neurodegeneration. In this scenario, evidence linking both autophagic and synaptic dysfunction to DEE provides the needed bridge between such pivotal processes for neuronal homeostasis and neurodegeneration. Furthermore, genetic defects affecting ion currents and cellular osmolarity, cytoskeletal structure and integrity of myelinated axons, neuronal morphology, and purine metabolism have been found to underlie DEE with progressive course. Recent evidence also demonstrates that neuroinflammation during gestation and in the immature brain can induce immune priming and increase the risk of developing DEEs. The phenotypic evolution of many DEEs beyond early childhood is still poorly understood and hardly preventable. Recent studies showed that DEEs, at least some of them, may be the consequence of early inflammatory and neurodegenerative dysfunctions with a variable severity determined by specific genetic and epigenetic factors. These findings open new avenues for uncovering the underpinnings of DEEs progression and symptomatology.
Indexed as
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41014440What Socratic holds
Registered trials
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 Socratic graph.