Peer-reviewed industrial hemp research papers, sorted by publication date. Browse the latest findings on hemp cultivation, processing, materials science, biomedical applications, and regulatory science from PubMed, OpenAlex, and other indexed sources.
Peer-reviewed industrial hemp research by Tommaso Lo Barco; Anna Kamińska; Roberta Solazzi; Claude Cancés; Giulia Barcia; Nicole Chémaly; Elena Fontana; Isabelle Desguerre; Laura Canafoglia; C. Hachon Le Camus published in Clinical Neurophysiology (2021).
Protocadherin 19 (PCDH19) gene is one of the most common genes involved in epilepsy syndromes. According to literature data PCDH19 is among the 6 genes most involved in genetic epilepsies. PCDH19 is located on chromosome Xq22.1 and is involved in neuronal connections and signal transduction. The most frequent clinical expression of PCDH19 mutation is epilepsy and mental retardation limited to female (EFMR) characterized by epileptic and non-epileptic symptoms affecting mainly females. However, t
Peer-reviewed industrial hemp research by Kim I. Bishop; Peter Κ. Isquith; Gérard A. Gioia; Kelly G. Knupp; Ingrid E. Scheffer; Rima Nabbout; Nicola Specchio; Joseph Sullivan; Stéphane Auvin; J. Helen Cross published in Epilepsy & Behavior (2022).
Innate immune response is one of our primary defenses against pathogens infection, although, if dysregulated, it represents the leading cause of chronic tissue inflammation. This dualism is even more present in the central nervous system, where neuroinflammation is both important for the activation of reparatory mechanisms and, at the same time, leads to the release of detrimental factors that induce neurons loss. Key players in modulating the neuroinflammatory response are mitochondria. Indeed,
These findings concur with previous observations that the majority of adult and pediatric patients continue to experience recurrent seizures and suffer from refractory epilepsy. Moderate to severe cognitive disability, loss of functional independence, and psychiatric disorders represent a hallmark of chronic NORSE signifying the major public health importance of this disorder.
Peer-reviewed industrial hemp research by Susanne Schubert‐Bast; Markus Wolff; Adelheid Wiemer‐Kruel; Sarah von Spiczak; Regina Trollmann; Philipp S. Reif; Clive Pritchard; Tilman Polster; Bernd A. Neubauer; Patrick May published in Epilepsy & Behavior (2019).
Peer-reviewed industrial hemp research by Damien Wright; Aisling Kenny; Sarah Eley; Andrew G. McKechanie; Andrew C. Stanfield published in Journal of Neurodevelopmental Disorders (2022).
Despite the availability of more than 30 antiseizure medications (ASMs), the proportion of patients who remain refractory to ASMs remains static. Refractory seizures are almost universal in patients with epileptic encephalopathies. Since many of these patients are not candidates for curative surgery, there is always a need for newer ASMs with better efficacy and safety profile. Recently, the anti-obesity medication fenfluramine (FFA) has been successfully repurposed, and various regulatory agenc
Epilepsy is a common, serious neurological disorder worldwide. Although this disease can be successfully treated in most cases, not all patients respond favorably to medical treatments, which can lead to pharmacoresistant epilepsy. Drug‑resistant epilepsy can be caused by a number of mechanisms that may involve environmental and genetic factors, as well as disease‑ and drug‑related factors. In recent years, numerous studies have demonstrated that genetic variation is involved in the drug resista
Voltage-gated sodium channels (Navs) are critical determinants of cellular excitability. These ion channels exist as large heteromultimeric structures and their activity is tightly controlled. In neurons, the isoform Na<sub>v</sub>1.6 is highly enriched at the axon initial segment and nodes, making it critical for the initiation and propagation of neuronal impulses. Changes in Na<sub>v</sub>1.6 expression and function profoundly impact the input-output properties of neurons in normal and patholo
Genetic sequencing technologies have led to an increase in the identification and characterization of monogenic epilepsy syndromes. This increase has, in turn, generated strong interest in developing "precision therapies" based on the unique molecular genetics of a given monogenic epilepsy syndrome. These therapies include diets, vitamins, cell-signaling regulators, ion channel modulators, repurposed medications, molecular chaperones, and gene therapies. In this review, we evaluate these therapi
<b>Background:</b> Epilepsy is the most common neurological manifestation in individuals with tuberous sclerosis complex (TSC). However, real-world evidence on diagnosis and treatment patterns is limited. Here, we present data from TuberOus Sclerosis registry to increase disease Awareness (TOSCA) on changes in patterns of epilepsy diagnosis, treatments, and outcomes over time, and detailed epilepsy characteristics from the epilepsy substudy. <b>Methods:</b> TuberOus Sclerosis registry to increas
Dravet syndrome (DS), previously known as severe myoclonic epilepsy of infancy, is a severe developmental and epileptic encephalopathy caused by loss-of-function mutations in one copy of <i>SCN1A</i> (haploinsufficiency), located on chromosome 2q24, with decreased function of Nav1.1 sodium channels in GABAergic inhibitory interneurons. Pharmacoresistant seizures in DS start in the infancy in the form of hemiclonic febrile status epilepticus. Later, other intractable seizure types develop includi
If ISS is suspected, electroencephalography (EEG) should be performed within a few days and, if confirmed, treatment should be initiated immediately. Response to first-line treatment should be evaluated clinically and electroencephalographically after 14 days. The preferred first-line treatment for ISS consists of either hormone-based monotherapy (AdrenoCorticoTropic Hormone [ACTH] or prednisolone) or a combination of hormone and vigabatrin. Children with tuberous sclerosis complex and those wit
Many animal prototypes illustrating the various attributes of human temporal lobe epilepsy (TLE) are available. These models have been invaluable for comprehending multiple epileptogenic processes, modifications in electrophysiological properties, neuronal hyperexcitability, neurodegeneration, neural plasticity, and chronic neuroinflammation in TLE. Some models have also uncovered the efficacy of new antiepileptic drugs or biologics for alleviating epileptogenesis, cognitive impairments, or spon
Major depressive disorder (MDD) is the foremost cause of global disability, being responsible for enormous personal, societal, and economical costs. Importantly, existing pharmacological treatments for MDD are partially or totally ineffective in a large segment of patients. As such, the search for novel antidepressant drug targets, anchored on a clear understanding of the etiological and pathophysiological mechanisms underpinning MDD, becomes of the utmost importance. The adenosinergic system, a
This review aims to provide an updated perspective of epilepsy genetics and precision medicine in adult patients, with special focus on developmental and epileptic encephalopathies (DEEs), covering relevant and controversial issues, such as defining candidates for genetic testing, which genetic tests to request and how to interpret them. A literature review was conducted, including findings in the discussion and recommendations. DEEs are wide and phenotypically heterogeneous electroclinical synd
The recurrent SCN1A p.R1636Q variant causes a clinical entity with a wider clinical spectrum than previously reported, characterized by neonatal onset epilepsy and absence of prominent movement disorder. Functional consequences of this variant lead to mixed loss and gain of function that is partially corrected by oxcarbazepine. The recurrent p.R1636Q variant represents one of the most common causes of early onset SCN1A-related epilepsies with separate treatment and prognosis implications.
We recommend clinicians to include <i>HCN</i> genes in epilepsy gene panels. Researchers should explore the possible underlying mechanisms for GOF and LOF variants by identifying the specific neuronal subtypes and neuroanatomical locations of each identified pathogenic variant. Researchers should identify specific HCN channel openers and blockers with high binding affinity. Such information will give clarity to the involvement of HCN channelopathies in epilepsy and provide the opportunity to dev
The neurobiological mechanism of post-traumatic stress disorder (PTSD) is poorly understood. The inhibition of GABA neurons, especially in the amygdala, is crucial for the precise regulation of the consolidation, expression, and extinction of fear conditioning. The GABAergic system is involved in the pathophysiological process of PTSD, with several studies demonstrating that the function of the GABAergic system decreases in PTSD patients. This paper reviews the preclinical and clinical studies,