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Journal of Experimental Neurology
ISSN: 2692-2819
2026
Volume 7, Issue 3, p101-140
Articles published in this issue are Open Access and licensed under Creative Commons Attribution License (CC BY NC) where the readers can reuse, download, distribute the article in whole or part by mentioning proper credits to the authors.
Beyond Clinical Trials: Perampanel across the Lifespan in Contemporary Epilepsy Practice
Anita N. Datta
Perampanel (PER) occupies a singular place in anti-seizure pharmacology. As the only anti-seizure medication (ASM) that acts through selective, non-competitive blockade of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, the principal mediators of fast excitatory neurotransmission in the brain, it brings a mechanistic distinctiveness that sets it apart from agents targeting sodium channels, calcium currents, or synaptic vesicle proteins
J Exp Neurol, 2026, Volume 7, Issue 3, p101-108 | DOI: 10.33696/Neurol.7.134
Demyelinating Polyneuropathy as the Initial Presentation of Poems Syndrome. The Challenge of Early Diagnosis. A Case Report and Literature Review
Danny Sameh Darwich, Fawaz Ghouse, Adel Kanaan, Shalini Cherala
POEMS syndrome is a rare paraneoplastic multisystemic disorder caused by an underlying monoclonal plasma-cell dyscrasia and characterized by Polyneuropathy, Organomegaly, Endocrinopathy, Monoclonal plasma cell disorder, and Skin changes. Because early manifestations often overlap with other conditions such as chronic inflammatory demyelinating polyneuropathy (CIDP) and multiple myeloma, diagnosis is frequently delayed.
J Exp Neurol, 2026, Volume 7, Issue 3, p109-119 | DOI: 10.33696/Neurol.7.135
The Cost of Safety: Balancing Biosafety and Histologic Integrity in Prion Research
Alyssa Seerley, Andrea Grindeland Panter
Prion diseases, or transmissible spongiform encephalopathies (TSEs), represent a group of incurable and invariably fatal neurodegenerative disorders driven by the pathological misfolding of the prion protein (PrP) [1–6]. These diseases are characterized by a progressive clinical course and, despite their significant impact on human [7–17] and animal [1,10,18–30] health, currently lack effective therapeutic interventions [31–34] and are limited in early-stage diagnostics [1,7,31–33]. Given the broad host range of prion diseases, together with the absence of effective treatments and limited antemortem diagnostic options, continued prion disease research remains essential.
J Exp Neurol, 2026, Volume 7, Issue 3, p120-124 | DOI: 10.33696/Neurol.7.136
Extracellular Vesicles in Angelman Syndrome: Expanding UBE3A Role beyond a Cell Autonomous Mechanism
Eduardo Penna, Michel Baudry, Xiaoning Bi
Angelman syndrome (AS) is a severe neurodevelopmental disorder caused by the loss of maternal UBE3A, an E3 ubiquitin ligase essential for neuronal development, synaptic plasticity, and cognitive function. AS has traditionally been viewed as a cell-autonomous disorder in which intracellular UBE3A deficiency drives neuronal dysfunction. However, recent evidence suggests that impaired extracellular vesicle (EV)-mediated intercellular communication also contributes to disease pathophysiology.
J Exp Neurol, 2026, Volume 7, Issue 3, p125-134 | DOI: 10.33696/Neurol.7.137
Commentary: Does First-Line Treatment Impact Outcomes in Trisomy 21-Associated Infantile Epileptic Spasms Syndrome?
Muzna AlFarsi, Anita N. Datta
Trisomy 21 (T21) is the most common chromosomal disorder and is associated with a substantially increased risk of epilepsy, affecting approximately 5–10% of children [1,2]. Among infants with T21, infantile epileptic spasms syndrome (IESS) is the most common epilepsy syndrome of the first year of life, with a reported prevalence of 0.6–13%, approximately 100-fold higher than in the general population [3,4]. The occurrence of IESS adds an additional burden to a population already at risk for neurodevelopmental impairment, making early recognition and effective treatment particularly important [2,5,6].
J Exp Neurol, 2026, Volume 7, Issue 3, p135-140 | DOI: 10.33696/Neurol.7.138
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