{"title":"Psychedelics and substance use disorder treatment.","authors":"Caitlin M DuPont, Matthew W Johnson","doi":"10.1016/bs.irn.2025.03.005","DOIUrl":"10.1016/bs.irn.2025.03.005","url":null,"abstract":"<p><p>The current chapter presents the literature evaluating the effects of classic psychedelic treatments on five substance use disorders: alcohol, tobacco, opioid, stimulant, and cannabis. Most work on psychedelics and substance use disorders was conducted for alcohol use disorder. A range of classic psychedelics (LSD, psilocybin, and ayahuasca) appear to be beneficial for facilitating both reduced drinking and abstinence. Small clinical trials have also shown promising initial results for both tobacco and opioid use disorders. In contrast, no trials have yet been conducted for stimulant and cannabis use disorders. Furthermore, the majority of studies described are naturalistic observational studies or correlational survey data. However, if such observational studies reflect causal therapeutic potential, these studies, combined with clinical trials, suggest potential broad transdiagnostic efficacy of psychedelics across multiple addictive drugs. The transdiagnostic effects of psychedelics are likely due to a combination of biological and psychological factors. Biologically, psychedelics appear to ameliorate deficits in brain areas involved in reward and emotional processing, which may reduce the risk of relapse. Psychologically, the insights gained during a psychedelic experience may reinforce personal motivations for sobriety and support subsequent behavior change. Overall, more work is needed to better characterize the potential benefits and limitations of psychedelic treatment for substance use disorders.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"181 ","pages":"305-327"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144337324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sally Spendiff, Hanns Lochmüller, Ricardo A Maselli
{"title":"Congenital myasthenic syndromes.","authors":"Sally Spendiff, Hanns Lochmüller, Ricardo A Maselli","doi":"10.1016/bs.irn.2025.04.025","DOIUrl":"https://doi.org/10.1016/bs.irn.2025.04.025","url":null,"abstract":"<p><p>Congenital myasthenic syndromes (CMS) result from impaired neuromuscular transmission and are due to genetic mutations in one of several genes involved in the development, function, or maintenance of the neuromuscular junction (NMJ). The clinical presentation, age of onset, and prognosis can vary significantly depending on the underlying genetic defect. Since therapeutic management should be tailored to the specific causative mutation, achieving an accurate diagnosis is essential for optimal patient care. This review summarizes the common diagnostic tests used for CMS and highlights critical features that help differentiate it from other conditions with similar presentations. Key clinical and diagnostic findings are discussed to guide clinicians in identifying potential causative mutations. Finally, we review current treatment options and explore emerging therapies that hold promise for improving patient outcomes.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"182 ","pages":"253-274"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144661423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Lambert Eaton Myasthenic Syndrome.","authors":"Shadi El-Wahsh, Stephen Reddel","doi":"10.1016/bs.irn.2025.04.027","DOIUrl":"https://doi.org/10.1016/bs.irn.2025.04.027","url":null,"abstract":"<p><p>Lambert Eaton Myasthenic Syndrome (LEMS) is a pre-synaptic neuromuscular junction disorder characterised clinically by leg-predominant proximal weakness with spread of weakness distally and cranially with increasing severity as well as reduced reflexes and autonomic symptoms such as a dry mouth. Typical electrophysiological findings include small compound muscle action potentials at rest that augment following short exercise, decrement at low frequency (2-5 Hz) repetitive nerve stimulation, and increment at high frequency (20-50 Hz) repetitive nerve stimulation. Immunologically, antibodies to voltage gated calcium channels are present in the majority of patients. LEMS is associated with small cell lung cancer (SCLC), or rarely other tumours, in approximately 50 % of cases, for which patients should be carefully screened. The synaptic physiology of LEMS demonstrates a reduction in the probability of pre-synaptic acetylcholine vesicle release. This results in a reduced number (reduced quantal content) of miniature endplate potentials such that the post-synaptic summative endplate potential is insufficient to trigger myofiber contraction, manifesting as weakness. The clinical electrophysiological findings reflect normal rate-dependent changes at a neuromuscular junction, in the context of a reduction in quantal release. Treatment of LEMS comprises symptomatic treatments such as 3,4 diaminopyridine (amifampridine), which increases quantal release; immunotherapy; and treatment of underlying malignancy if present. The life expectancy of non-tumour LEMS is normal, although complete remission is uncommon. Progression of SCLC determines prognosis in tumour-associated LEMS, which is nonetheless better than in SCLC without LEMS.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"182 ","pages":"227-251"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144661426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cognitive and affective models of psychedelics in rodents.","authors":"Dasha Anderson, Emma S J Robinson","doi":"10.1016/bs.irn.2025.02.002","DOIUrl":"10.1016/bs.irn.2025.02.002","url":null,"abstract":"<p><p>In recent years, public and academic interest into psychedelics has increased, given the clinical evidence of their potential benefits for treating psychiatric conditions such as major depressive disorder (MDD). While this has been accompanied by several landmark human studies, mechanistic studies in rodents are still relatively few, but such studies are crucial for understanding the neurobiological underpinnings of the therapeutic effects of psychedelics. However, findings from rodent studies will only be of benefit to patients if they achieve translational validity. In this chapter, we will critically appraise rodent assays traditionally used to study cognition and affect, summarising existing findings with psychedelics. We will also highlight novel, translationally valid assays that have already been used or could be used in the future to study these drugs. We argue that the adoption of translational assays is critical for the interpretation of animal studies of psychedelic effects on cognition and affect. We also discuss how these studies have the potential to help unravel the mechanisms which contribute to their therapeutic effects but only if they involve relevant doses.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"181 ","pages":"77-98"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144337315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Introduction: Approved treatments for alcohol use disorder by regulatory agencies.","authors":"Rosana Camarini, Fábio Cardoso Cruz","doi":"10.1016/bs.irn.2024.07.001","DOIUrl":"https://doi.org/10.1016/bs.irn.2024.07.001","url":null,"abstract":"<p><p>Alcohol, the most widely consumed substance globally, can lead to severe adverse effects for both users and those around them. Chronic ethanol consumption may lead to alcohol use disorder (AUD), a chronic relapsing condition characterized by compulsive drinking despite negative consequences. AUD is marked by a high relapse rate among individuals attempting abstinence. Currently, only a few medications, such as disulfiram, naltrexone, nalmefene, and acamprosate, are approved to treat AUD. Moreover, genetic factors and comorbid conditions can significantly influence both the development of AUD and the efficacy of its treatment. This chapter explores the genetic underpinnings of AUD and reviews the main pharmacological treatments available for managing this disorder.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"178 ","pages":"1-22"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142635036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Javiera Gallardo, Pablo Berríos-Cárcamo, Fernando Ezquer
{"title":"Mesenchymal stem cells as a promising therapy for alcohol use disorder.","authors":"Javiera Gallardo, Pablo Berríos-Cárcamo, Fernando Ezquer","doi":"10.1016/bs.irn.2024.07.002","DOIUrl":"https://doi.org/10.1016/bs.irn.2024.07.002","url":null,"abstract":"<p><p>Alcohol Use Disorder (AUD) is a highly prevalent medical condition characterized by impaired control over alcohol consumption, despite negative consequences on the individual's daily life and health. There is increasing evidence suggesting that chronic alcohol intake, like other addictive drugs, induces neuroinflammation and oxidative stress, disrupting glutamate homeostasis in the main brain areas related to drug addiction. This review explores the potential application of mesenchymal stem cells (MSCs)-based therapy for the treatment of AUD. MSCs secrete a broad array of anti-inflammatory and antioxidant molecules, thus, the administration of MSCs, or their secretome, could reduce neuroinflammation and oxidative stress in the brain. These effects correlate with an increase in the expression of the main glutamate transporter, GLT1, which, through the normalization of the extracellular glutamate levels, could mediate the inhibitory effect of MSCs' secretome on chronic alcohol consumption, thus highlighting GLT1 as a central target to reduce chronic alcohol consumption.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"178 ","pages":"179-211"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142635039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Preface.","authors":"Rosana Camarini, Fábio C Cruz","doi":"10.1016/S0074-7742(24)00138-7","DOIUrl":"https://doi.org/10.1016/S0074-7742(24)00138-7","url":null,"abstract":"","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"178 ","pages":"xix-xxii"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142635045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Insight gained from using animal models to study pain in Parkinson's disease.","authors":"Yazead Buhidma, Joana Lama, Susan Duty","doi":"10.1016/bs.irn.2023.08.013","DOIUrl":"10.1016/bs.irn.2023.08.013","url":null,"abstract":"<p><p>Pain is one of the key non-motor symptoms experienced by a large proportion of people living with Parkinson's disease (PD), yet the mechanisms behind this pain remain elusive and as such its treatment remains suboptimal. It is hoped that through the study of animal models of PD, we can start to unravel some of the contributory mechanisms, and perhaps identify models that prove useful as test beds for assessing the efficacy of potential new analgesics. However, just how far along this journey are we right now? Is it even possible to model pain in PD in animal models of the disease? And have we gathered any insight into pain mechanisms from the use of animal models of PD so far? In this chapter we intend to address these questions and in particular highlight the findings generated by others, and our own group, following studies in a range of rodent models of PD.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"174 ","pages":"99-118"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139716765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Steve Vucic, Mamede de Carvalho, James Bashford, James J P Alix
{"title":"Contribution of neurophysiology to the diagnosis and monitoring of ALS.","authors":"Steve Vucic, Mamede de Carvalho, James Bashford, James J P Alix","doi":"10.1016/bs.irn.2024.04.001","DOIUrl":"10.1016/bs.irn.2024.04.001","url":null,"abstract":"<p><p>This chapter describes the role of neurophysiological techniques in diagnosing and monitoring amyotrophic lateral sclerosis (ALS). Despite many advances, electromyography (EMG) remains a keystone investigation from which to build support for a diagnosis of ALS, demonstrating the pathophysiological processes of motor unit hyperexcitability, denervation and reinnervation. We consider development of the different diagnostic criteria and the role of EMG therein. While not formally recognised by established diagnostic criteria, we discuss the pioneering studies that have demonstrated the diagnostic potential of transcranial magnetic stimulation (TMS) of the motor cortex and highlight the growing evidence for TMS in the diagnostic process. Finally, accurately monitoring disease progression is crucial for the successful implementation of clinical trials. Neurophysiological measures of disease state have been incorporated into clinical trials for over 20 years and we review prominent techniques for assessing disease progression.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"176 ","pages":"87-118"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141159321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tobias Moll, Calum Harvey, Elham Alhathli, Sarah Gornall, David O'Brien, Johnathan Cooper-Knock
{"title":"Non-coding genome contribution to ALS.","authors":"Tobias Moll, Calum Harvey, Elham Alhathli, Sarah Gornall, David O'Brien, Johnathan Cooper-Knock","doi":"10.1016/bs.irn.2024.04.002","DOIUrl":"10.1016/bs.irn.2024.04.002","url":null,"abstract":"<p><p>The majority of amyotrophic lateral sclerosis (ALS) is caused by a complex gene-environment interaction. Despite high estimates of heritability, the genetic basis of disease in the majority of ALS patients are unknown. This limits the development of targeted genetic therapies which require an understanding of patient-specific genetic drivers. There is good evidence that the majority of these missing genetic risk factors are likely to be found within the non-coding genome. However, a major challenge in the discovery of non-coding risk variants is determining which variants are functional in which specific CNS cell type. We summarise current discoveries of ALS-associated genetic drivers within the non-coding genome and we make the case that improved cell-specific annotation of genomic function is required to advance this field, particularly via single-cell epigenetic profiling and spatial transcriptomics. We highlight the example of TBK1 where an apparent paradox exists between pathogenic coding variants which cause loss of protein function, and protective non-coding variants which cause reduced gene expression; the paradox is resolved when it is understood that the non-coding variants are acting primarily via change in gene expression within microglia, and the effect of coding variants is most prominent in neurons. We propose that cell-specific functional annotation of ALS-associated genetic variants will accelerate discovery of the genetic architecture underpinning disease in the vast majority of patients.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"176 ","pages":"75-86"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141159333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}