International Review Of Neurobiology[JOURNAL]
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200 papers
Thymic physiology and pathophysiology in Myasthenia Gravis.
Dragin N, Le Panse R
Int Rev Neurobiol · 2025 · PMID 40675741 · Publisher ↗
The thymus is a central lymphoid organ responsible for T-cell development and maturation and is crucial in adaptive immunity. This organ creates a specialized environment for thymocyte differentiation and positive/negati...
The thymus is a central lymphoid organ responsible for T-cell development and maturation and is crucial in adaptive immunity. This organ creates a specialized environment for thymocyte differentiation and positive/negative selection, ensuring the survival of functional and self-tolerant T cells while eliminating autoreactive clones. This process, which is known as T-cell education, involves interactions between developing T cells and stromal cells, primarily thymic epithelial cells, which present tissue-specific antigens. Proper thymus function remains vital for maintaining immune homeostasis. However, thymic abnormalities have been implicated in Myasthenia Gravis (MG), where the thymus often exhibits lymphofollicular hyperplasia or thymomas, which may trigger an autoimmune response against the acetylcholine receptor at the neuromuscular junction. This leads to impaired neuromuscular transmission and characteristic muscle weakness. Understanding the etiological mechanisms underlying thymic alterations associated with MG is crucial for elucidating immune dysregulation resulting from an abnormal thymus, which may persist even post-therapeutic thymectomy.
Contribution of cellular immune dysregulation to myasthenia gravis pathology.
Bayer AC, Nowak RJ, O'Connor KC
Int Rev Neurobiol · 2025 · PMID 40675740 · Publisher ↗
Myasthenia gravis (MG) is an autoimmune disorder in which autoantibodies attack proteins at the neuromuscular junction, resulting in impaired neuromuscular transmission. Like other autoimmune diseases, MG arises when the...
Myasthenia gravis (MG) is an autoimmune disorder in which autoantibodies attack proteins at the neuromuscular junction, resulting in impaired neuromuscular transmission. Like other autoimmune diseases, MG arises when the immune system fails to distinguish self from non-self, attacking and damaging normal tissues. The pathological response involves not only B cells, responsible for autoantibody production, but also T cells, which provide essential support for B cell pathogenicity. While the precise triggers of this abnormal immune response remain undefined, MG is recognized as a multifactorial disease influenced by immune dysregulation along with genetic and environmental factors. This chapter explores the complex immunopathology of MG, highlighting how these factors collectively contribute to disease development. We examine the physiological development of T and B cell compartments, the tolerance checkpoints designed to prevent autoimmunity, and the consequences of their failure. Finally, we discuss the dysregulation of these cellular compartments in MG, emphasizing their roles in disease progression, the persistence of autoimmunity, and responses to treatment.
Congenital myasthenic syndromes.
Spendiff S, Lochmüller H, Maselli RA
Int Rev Neurobiol · 2025 · PMID 40675739 · Publisher ↗
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 ju...
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.
Lambert Eaton Myasthenic Syndrome.
El-Wahsh S, Reddel S
Int Rev Neurobiol · 2025 · PMID 40675738 · Publisher ↗
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 seve...
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.
Neuromuscular junction and the complement system.
Jacob S, Howard JF
Int Rev Neurobiol · 2025 · PMID 40675737 · Publisher ↗
Nearly 90 % of generalized myasthenia gravis (MG) patients have IgG1 or IgG3 antibodies against the acetylcholine receptor (AChR). Acetylcholine receptor antibodies induce neuromuscular transmission defect by various pot...
Nearly 90 % of generalized myasthenia gravis (MG) patients have IgG1 or IgG3 antibodies against the acetylcholine receptor (AChR). Acetylcholine receptor antibodies induce neuromuscular transmission defect by various potential mechanisms including internalisation of AChR, receptor blockade and by activation of the classical complement pathway. Membrane attack complex (MAC) which is the final end product of complement activation leads to architectural destruction of the neuromuscular junction (NMJ). Several experimental models (EAMG) have shown evidence for complement in the pathogenesis of MG, with demonstration of prevention or reversal of the disease using complement inhibitory therapies. Various molecules that target the complement system have been developed to treat myasthenia gravis. Most of the currently studied molecules inhibit complement protein 5 (C5), which prevents the formation of MAC and subsequent NMJ destruction. The currently studied anti-complement therapies for MG include eculizumab, zilucoplan, ravulizumab, pozelimab, cemdisiran, gefurilimab, danicopan and few others in the pipeline. Many of these have also been shown to have long term benefit in different sub-groups of patients with MG. Given the risk of Gram-negative septicaemia (especially by meningococcus), patients would need vaccination prior to initiation of treatment and in some countries prophylactic antibiotics during treatment is recommended, although no major safety signatures have been noted in the studies so far. Future studies identifying specific biomarkers might help clinicians select the most appropriate patients who are more likely to respond to complement inhibitory therapies.
Blood and digital biomarkers in MG.
Bhandage AK, Chen J, Kaminski HJ … +1 more , Punga AR
Int Rev Neurobiol · 2025 · PMID 40675736 · Publisher ↗
Biomarkers are measurable indicators to assess physiological processes, disease states, or therapy responses. In myasthenia gravis (MG), biomarkers are critical for diagnosis, monitoring, and treatment optimization. Desp...
Biomarkers are measurable indicators to assess physiological processes, disease states, or therapy responses. In myasthenia gravis (MG), biomarkers are critical for diagnosis, monitoring, and treatment optimization. Despite advances in MG diagnostics and therapies, predictive biomarkers to personalize treatment remain underdeveloped. Key diagnostic blood biomarkers include antibodies against acetylcholine receptors (AChR) or muscle-specific tyrosine kinase (MuSK), confirming MG diagnosis and guiding treatment decisions. Prognostic markers, such as microRNAs (e.g., miR-150-5p and miR-30e-5p), show promise in predicting disease progression. Pharmacodynamic biomarkers enhance treatment precision, including CD20+ B cell counts for Rituximab and the CYP3A5 gene for Tacrolimus. Emerging research on metabolites, T and B-cell markers, complement factors, and proteomics may help distinguish MG's autoimmune profile. Digital biomarkers, using wearables and sensors, offer innovative patient monitoring. Future efforts integrating multi-omics and big data could revolutionize biomarker discovery, advancing personalized care and improving outcomes for MG patients.
Special populations in myasthenia gravis: Early, late, and very late-onset MG.
Hoffmann S
Int Rev Neurobiol · 2025 · PMID 40675735 · Publisher ↗
The age at disease onset significantly influences the clinical course, pathophysiology, and treatment response in Myasthenia Gravis (MG). This chapter examines how immunological profiles, autoantibody prevalence, thymic...
The age at disease onset significantly influences the clinical course, pathophysiology, and treatment response in Myasthenia Gravis (MG). This chapter examines how immunological profiles, autoantibody prevalence, thymic pathology, genetic associations, treatment responses, and disease severity vary across early-onset (EOMG), late-onset (LOMG), and very late-onset MG (VLOMG). EOMG often presents with distinct immunological and genetic profiles, a predominance of female patients, and a higher incidence of thymic hyperplasia. In contrast, LOMG and VLOMG are characterized by thymic atrophy, differing genetic associations, and milder long-term disease courses with variable treatment responses. Recognizing these age-related variations is essential for optimizing diagnostic approaches and therapeutic strategies, highlighting the need for individualized patient management across different age groups.
Epidemiology of myasthenia gravis.
Gilhus NE, Breiner A
Int Rev Neurobiol · 2025 · PMID 40675734 · Publisher ↗
MG epidemiology may provide clues to disease etiology and pathogenesis. It is crucial for health planning and to estimate societal needs for health care resources. Recent high-quality studies have found an annual MG inci...
MG epidemiology may provide clues to disease etiology and pathogenesis. It is crucial for health planning and to estimate societal needs for health care resources. Recent high-quality studies have found an annual MG incidence of approximately 20 per million person-years, and a prevalence of approximately 25 per 100,000 population. Geographical variation reflects differences in case finding and diagnostic tools, but also a multitude of genetic and environmental etiological and risk factors. MG prevalence has increased in recent years because of more elderly people in the general population, improved case finding, and improved MG treatment with reduced mortality. In populations with optimal treatment, there is only a slightly increased mortality risk with MG. There are marked variations among MG disease subgroups regarding epidemiology. MuSK MG is more common in the Mediterranean area, juvenile MG is most common in China, whereas late onset MG with AChR antibodies is a subtype that has increased in incidence and prevalence globally.
Animal models of myasthenia gravis.
Sikorski PM, Kusner LL
Int Rev Neurobiol · 2025 · PMID 40675733 · Publisher ↗
Animal models offer a platform to advance our understanding of myasthenia gravis (MG), an autoimmune disorder characterized by impaired neuromuscular transmission. Experimental autoimmune MG models (EAMG) actively induce...
Animal models offer a platform to advance our understanding of myasthenia gravis (MG), an autoimmune disorder characterized by impaired neuromuscular transmission. Experimental autoimmune MG models (EAMG) actively induce autoimmunity through antigen immunization, aiding in understanding the immune response to self. Passive transfer models (PTMG) involve the injection of pathogenic antibodies into animals, providing insights into antibody-mediated mechanisms and complement-driven damage to the neuromuscular junction (NMJ). The pathogenic effect of autoantibodies targeting acetylcholine receptors (AChR), muscle-specific kinase (MuSK), and low-density lipoprotein receptor-related protein 4 (Lrp4) results in changes to the NMJ that are mechanistically distinct. These models validate therapeutic interventions preclinically, with methodologies ranging from antibody transfer to genetic modifications. Despite the translational challenges, these models bridge preclinical research and clinical applications, enabling the development of targeted treatments for MG.
Cell models for studying myasthenia gravis.
Huang YF, Verpalen RLK, Punga AR … +1 more , Huijbers MG
Int Rev Neurobiol · 2025 · PMID 40675732 · Publisher ↗
Understanding the pathophysiology of Myasthenia Gravis (MG) and developing effective treatments requires using cell models that replicate key features of the disease, particularly those involved in the autoimmune respons...
Understanding the pathophysiology of Myasthenia Gravis (MG) and developing effective treatments requires using cell models that replicate key features of the disease, particularly those involved in the autoimmune response and neuromuscular dysfunction. This chapter reviews the various cell-based models used in MG research and those with potential for preclinical MG studies, including muscle cells and co-culture models to form neuromuscular junctions (NMJ). We discuss the strengths and limitations of these models, further outline methods for characterizing these, and provide an outlook on the future refinement and abilities of cell models for advancing MG research.
Structure and function of the neuromuscular junction in health and myasthenia gravis.
Plomp JJ, Webster RG
Int Rev Neurobiol · 2025 · PMID 40675731 · Publisher ↗
The neuromuscular junction (NMJ) connects a motor neuron to a skeletal muscle cell. Cholinergic synaptic transmission enables muscle contraction, which is crucial for survival. Although synaptic communication at the NMJ...
The neuromuscular junction (NMJ) connects a motor neuron to a skeletal muscle cell. Cholinergic synaptic transmission enables muscle contraction, which is crucial for survival. Although synaptic communication at the NMJ is robust, with an inherent safety margin, it becomes hampered in the neuro-immunological disorder myasthenia gravis (MG). The synaptic dysfunction underlies the (fatigable) muscle weakness, which hallmarks this disease. In this chapter, we will review normal NMJ physiology and the pathophysiological consequences of autoimmune attacks in MG, focusing on recent insights and developments.
Preface.
Nutt DJ, Thurgur H
Int Rev Neurobiol · 2025 · PMID 40541322 · Publisher ↗
Abstract loading — click title to view on PubMed.
Foreword.
Schlag AK, Nutt DJ, Lynskey MT
Int Rev Neurobiol · 2025 · PMID 40541321 · Publisher ↗
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Clinical pharmacology.
Vogt SB, Liechti ME
Int Rev Neurobiol · 2025 · PMID 40541320 · Publisher ↗
To design therapeutic trials and select the most appropriate substance and dose for an indication, a detailed understanding of clinical pharmacology is crucial. In recent years, several studies have explored the human ph...
To design therapeutic trials and select the most appropriate substance and dose for an indication, a detailed understanding of clinical pharmacology is crucial. In recent years, several studies have explored the human pharmacology of different psychedelics and 3,4-methylendioxymethylamphetamin (MDMA). This chapter summarizes pharmacological characteristics of the serotonergic psychedelics psilocybin, lysergic acid diethylamide (LSD), mescaline, N,N-dimethyltryptamine (DMT), 5-methoxy-DMT (5-MeO-DMT), and MDMA. We summarize their mechanisms of action, pharmacokinetics, pharmacodynamics, metabolism, and safety, with a focus on human data from modern clinical trials. Additionally, we provide recommendations for dosing, dose adjustment, and interactions with other medications. We show that the different serotonergic psychedelics produce overall comparable acute subjective and somatic effects primarily through interactions with 5-HT receptors. However, the exact mechanisms of their potential therapeutic benefits in patients remain to be elucidated. Moreover, classic psychedelics differ substantially in their pharmacokinetics and metabolism, resulting mainly in different durations of action, which may influence their suitability for specific therapeutic uses and indications. In contrast, MDMA has a psychopharmacological profile that is distinct from serotonergic psychedelics, characterized by acute stimulant-like and empathogenic effects. In terms of pharmacokinetic-pharmacodynamic relationships, acute effects of the psychedelics mirror their plasma-concentration-time curves, whereas acute effects of MDMA are shorter-lasting than its presence in the body. Thus, MDMA, but not the psychedelics, exhibits marked acute pharmacological tolerance. A good understanding of the pharmacology of classic psychedelics and MDMA forms the basis for their clinical use and the design of clinical therapeutic trials.
Cognitive and affective models of psychedelics in rodents.
Anderson D, Robinson ESJ
Int Rev Neurobiol · 2025 · PMID 40541319 · Publisher ↗
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 th...
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.
Serotonin, immune function, and psychedelics as potent anti-inflammatories.
Nichols CD, Foster TP
Int Rev Neurobiol · 2025 · PMID 40541318 · Publisher ↗
Psychedelics are primarily recognized for their profound behavioral effects, leading most research on psychedelics and their primary target, the 5-HT receptor, to focus on brain activity. However, these receptors are not...
Psychedelics are primarily recognized for their profound behavioral effects, leading most research on psychedelics and their primary target, the 5-HT receptor, to focus on brain activity. However, these receptors are not only found within the brain and are present in nearly every tissue and cell type throughout the body, playing a significant role alongside serotonin in modulating various processes, including immune function. Serotonin acting at 5-HT receptors generally promotes inflammation. Levels are elevated at sites of inflammation and through 5-HT receptor activation lead to events including increased cytokine production, eosinophil recruitment, T-cell activation, and mast cell degranulation. Some psychedelics, but not all, have been found to have powerful anti-inflammatory and immunomodulatory effects through activation of 5-HT2A receptors in preclinical experimental systems and models of human inflammatory diseases. Human studies examining anti-inflammatory effects of psychedelics are limited but suggestive that psychedelics may represent a new strategy to treat inflammatory diseases. In this review we will present an overview of serotonergic modulation of immune function, the role of 5-HT2A receptors in these processes, and a summary of key findings with psychedelics with regards to anti-inflammatory efficacy.
The protective effect of DMT against neurodegeneration.
Frecska E, Kovács A, Szabo A
Int Rev Neurobiol · 2025 · PMID 40541317 · Publisher ↗
This paper explores the therapeutic potential of DMT in neuroprotective strategies, particularly concerning ischemia-reperfusion injury (IRI) and neurodegenerative disorders. Besides its potent serotonin receptor actions...
This paper explores the therapeutic potential of DMT in neuroprotective strategies, particularly concerning ischemia-reperfusion injury (IRI) and neurodegenerative disorders. Besides its potent serotonin receptor actions, DMT is also an endogenous agonist of the sigma-1 receptor (Sig-1R). Sigma receptors are a unique family of proteins with high expression in the brain and spinal cord and have been involved in the etiology, symptom course and treatment of several central nervous system disorders. Our previous theoretical and experimental work strongly suggest that targeting sigma (and serotonin) receptors via DMT may be particularly useful for treatment in a number of neurological conditions like stroke, global brain ischemia, Alzheimer's disease, and amyotrophic lateral sclerosis. In this article, we briefly overview the function of Sig1-R in cellular bioenergetics with a focus on the processes involved in IRI and summarize the results of our previous preclinical (in vitro and in vivo) DMT studies aiming at mitigating IRI and related cellular neuropathologies. We conclude that the effect of DMT may involve a universal role in cellular protective mechanisms suggesting therapeutic potentials against different components and types of IRIs emerging in local and generalized brain ischemia after stroke or cardiac arrest. The multiple neuroprotective mechanisms facilitated by DMT may position it as a model molecule for developing pharmacological treatments for neurodegenerative disorders.
Psychedelics for the treatment of end-of-life distress in patients with a life-threatening disease.
Tap S, Bostoen T, Breeksema J … +1 more , Schoevers R
Int Rev Neurobiol · 2025 · PMID 40541316 · Publisher ↗
Patients with a life-threatening disease (LTD) sometimes suffer from end-of-life distress (EOLD) which refers to the physical, psychological, emotional, and spiritual suffering related to chronic illness and the possibil...
Patients with a life-threatening disease (LTD) sometimes suffer from end-of-life distress (EOLD) which refers to the physical, psychological, emotional, and spiritual suffering related to chronic illness and the possibility of death. Palliative care interventions seek to improve the quality of life of patients with EOLD and their significant others. Currently, a range of psychological and pharmacological palliative care interventions may be used to mitigate the various symptoms related to EOLD. However, the evidence for their efficacy is inconclusive with only short- to moderate effects. Another significant and relevant limitation in the context of LTDs is that palliative care interventions often require months to take effect. In the past decade, psychedelic-assisted therapy (PAT) has been increasingly investigated for its therapeutic potential in addressing EOLD in various LTDs characterized by highly significant and sometimes sustained decreases in symptoms of depression and (death) anxiety along with other EOLD-related improvements (e.g., meaning, spiritual well-being, optimism, life satisfaction, and change attitudes towards LTDs). The current chapter will provide a detailed description of the concept of EOLD followed by estimated prevalence rates in a range of LTDs. Next, the chapter provides a brief overview of palliative interventions and their limitations. The chapter then introduces a description of PAT, its evidence-base, and why it seems to work in particular for patients with EOLD. The chapter is concluded with future perspectives.
Post-traumatic stress disorder in psychedelic research.
Bostoen T, Tap S, Breeksema J … +1 more , Schoevers R
Int Rev Neurobiol · 2025 · PMID 40541315 · Publisher ↗
Post-Traumatic Stress Disorder (PTSD) is a severe psychiatric condition that develops after exposure to trauma such as combat, natural disasters, or assault. It is characterized by re-experiencing trauma, avoidance, hype...
Post-Traumatic Stress Disorder (PTSD) is a severe psychiatric condition that develops after exposure to trauma such as combat, natural disasters, or assault. It is characterized by re-experiencing trauma, avoidance, hyperarousal, and negative alterations in cognition and mood. Since its formal inclusion in the Diagnostic and Statistical Manual of Mental Disorders (DSM)-III in 1980, PTSD has been extensively researched. Current guideline-recommended treatments include trauma-focused psychotherapies and medications. However, a significant proportion of patients show limited response to these treatments. Psychedelic-assisted therapies, particularly 3,4-Methylenedioxymethamphetamine (MDMA)-assisted therapy, offer an innovative approach for treating PTSD. Over the past two decades, MDMA-assisted therapy has emerged as one of the most promising psychedelic treatments, especially for patients resistant to conventional therapies. MDMA can enhance the processing of traumatic memories during psychotherapy and holds potential for other psychiatric disorders. Recent clinical trials highlight the effectiveness of MDMA-assisted therapy, demonstrating substantial and sustained reductions in PTSD symptoms. The FDA has designated MDMA-assisted therapy as a "breakthrough therapy" for PTSD in 2017. However, due to methodological concerns such as unblinding and potential expectancy effects, the FDA decided in 2024 not to approve MDMA- assisted therapy for clinical use, requiring additional research to address these issues. This chapter explores the clinical research on psychedelic-assisted therapies for PTSD, with a particular focus on MDMA-assisted therapy. It will examine the potential psychological and neurobiological mechanisms of action, as well as the methodological challenges and future directions in the field. The growing body of evidence supporting MDMA-assisted therapy for PTSD is promising, especially for individuals who have not responded to traditional treatments.
Psychedelics and substance use disorder treatment.
DuPont CM, Johnson MW
Int Rev Neurobiol · 2025 · PMID 40541314 · Publisher ↗
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 subst...
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.
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