Background: Psychedelics are increasingly recognized as a promising and innovative treatment strategy for several mental disorders. However, there is still a lively controversy in the medical community as regards the rationale of their employment, specifically their indications and potential dangers. Methods: A comprehensive literature search on “MEDLINE/PubMed” and “Web of Science” was performed from inception to 26 June 2024, cross-checking the obtained references. We included all studies, i.e., both clinical and preclinical, that supplied original data. Results: We initially obtained a total of 1083 entries, 813 from MEDLINE/PubMed and 270 from Web of Science. After duplicate elimination, 903 underwent systematic literature selection. Primary abstract screening yielded a total of 572 candidates for eligibility assessment and excluded 331 entries on formal grounds. Eligibility assessment led to the exclusion of 501 titles. Finally, a total of 70 articles were included in this review. Discussion: Preclinical evidence from genetic expression, histology and behavioral studies is soundly consistent with psychedelics possessing neuroplasticity-inducing properties. Despite methodological difficulties, clinical evidence seems to be inferentially in agreement with preclinical findings. However, it is still unclear whether the “neuroplastic boost” induced by classic psychedelics might be dissociable from the psychodysleptic effects, thereby reducing the psychopathological hazards implied by these compounds. Moreover, the fact that the so-called “relaxation of priors” should be unconditionally beneficial appears debatable, and further research should clarify the possible indications and contraindications of psychedelic psychoplastogens within a precision medicine perspective.

Background/Objectives: Obsessive–compulsive disorder (OCD) is a complex psychiatric condition often associated with alterations in cognitive processes, including memory. Although memory dysfunction has been proposed as a contributing factor to the onset and maintenance of OCD symptoms, it remains debated whether these deficits reflect genuine cognitive impairments or maladaptive metacognitive processes, such as pathological doubt and memory distrust. This review aims to synthesize current findings on memory functioning in OCD, focusing on distinct memory systems and the role of metacognition. Methods: A comprehensive literature search was conducted across five databases (PubMed, Scopus, Embase, PsycINFO, and Google Scholar), covering studies up to April 2025. Search terms included “Obsessive-compulsive disorder”; “OCD”; “Memory dysfunction”; “Episodic memory”; “Working memory impairment”; “Prospective memory deficits”; “Checking compulsions”; “Memory confidence”; “Cognitive biases”. Results: Short-term memory appears generally preserved in OCD. Working memory deficits are consistently reported, especially in the visuospatial domain, and they are associated with difficulties in updating and clearing irrelevant information. Episodic memory impairments are common and often linked to inefficient encoding strategies and heightened cognitive self-consciousness. Prospective memory is frequently compromised under neutral conditions. Individuals with checking symptoms tend to show intact objective memory performance, despite reporting low memory confidence, supporting the concept of memory distrust. Conclusions: Memory dysfunction in OCD is multifaceted, involving both cognitive and metacognitive alterations. The evidence supports a model in which executive dysfunctions and memory-related beliefs contribute to compulsive behaviors more than objective memory failure. These insights highlight the need for integrative assessment protocols and personalized interventions targeting both cognitive performance and metacognitive appraisals.

Background/Objectives: Sensory deprivation, defined as a reduction or absence of external sensory input across one or more modalities, has long been investigated in extreme and experimental settings. More recently, its relevance has expanded to clinical contexts and environmental conditions. The present narrative review aims to synthesize current evidence on the neurobiological mechanisms, psychological effects, and clinical implications of sensory deprivation, with particular attention to its dual role as both a risk factor and, under controlled conditions, a potential therapeutic tool. Methods: A narrative literature search was conducted using PubMed, Scopus, and PsycINFO, covering studies published up to August 2025. Search terms included sensory deprivation, neuroplasticity, neurotransmitters, HPA axis, neuro-inflammation, circadian rhythms, psychopathology, extreme environments, and spaceflight. Preclinical and clinical studies examining biological, cognitive, and psychological consequences of reduced sensory stimulation were included. Data were synthesized thematically without quantitative meta-analysis. Results: Evidence indicates that sensory deprivation induces widespread neurobiological adaptations involving neurotransmitter systems (particularly dopaminergic pathways), dysregulation of the hypothalamic–pituitary–adrenal axis, neuroimmune activation, circadian rhythm disruption, and structural and functional brain changes, notably affecting the hippocampus. These alterations are associated with increased vulnerability to depression, anxiety, hallucinations, dissociative symptoms, and cognitive impairment. Duration, voluntariness, and individual differences (e.g., baseline vulnerability/resilience, trait anxiety, and prior psychiatric history) critically modulate outcomes. However, short-term and voluntary sensory restriction, such as Floatation-REST, may promote relaxation and emotional regulation under specific conditions. Conclusions: Sensory deprivation exerts complex, context-dependent effects on brain function and mental health. Duration, individual vulnerability, and voluntariness critically modulate outcomes. Understanding these mechanisms is increasingly relevant for clinical practice and for developing preventive strategies in extreme environments, including future long-duration space missions.

Background/Objectives: Major depressive disorder (MDD) represents a leading cause of global disability, with approximately one-third of patients exhibiting treatment resistance (TRD) despite adequate pharmacological interventions. This treatment gap underscores the urgent need for novel therapeutic strategies. Recently, a series of data suggests that botulinum neurotoxin of type A (BoNT-A), traditionally used for neuromuscular and cosmetic indications, could constitute a potential antidepressant tool. This narrative review critically examines the current preclinical and clinical findings of BoNT-A in MDD. Methods: A comprehensive search of PubMed, Scopus, and Web of Science was conducted up to June 2025, including randomized controlled trials, observational studies, animal models, and mechanistic investigations. Search terms included “Botulinum Toxin,” “BoNT type A”, “Depression”, “Major Depressive Disorder”, “Facial Feedback”, and “Neurobiology”. Results: Some randomized and observational studies would indicate that glabellar BoNT-A injections might lead to significant reductions in depressive symptoms in patients with MDD and TRD. Proposed mechanisms include both peripheral modulation of emotional expression and brain effects, such as reduced amygdala hyperactivity, increased BDNF expression, and enhanced monoaminergic transmission. Preclinical studies confirm that BoNT-A modulates limbic and brainstem circuits, possibly implicated in affective regulation. The few comparative studies suggest therapeutic efficacy comparable to that of SSRIs, with a more rapid onset. Preliminary data also support its application in bipolar depression and comorbid anxiety disorders. Conclusions: The available literature would indicate that BoNT-A might constitute a promising candidate at least as an adjunctive treatment in MDD, although the impact of current findings is limited due to the methodological heterogeneity and the small sample sizes of patients examined. Further large-scale, placebo-controlled trials are warranted to elucidate the mode of action of BoNT-A and to validate or not its clinical effectiveness.

Background/Objectives: Major depressive disorder (MDD) represents a leading cause of global disability, with approximately one-third of patients exhibiting treatment resistance (TRD) despite adequate pharmacological interventions. This treatment gap underscores the urgent need for novel therapeutic strategies. Recently, a series of data suggests that botulinum neurotoxin of type A (BoNT-A), traditionally used for neuromuscular and cosmetic indications, could constitute a potential antidepressant tool. This narrative review critically examines the current preclinical and clinical findings of BoNT-A in MDD. Methods: A comprehensive search of PubMed, Scopus, and Web of Science was conducted up to June 2025, including randomized controlled trials, observational studies, animal models, and mechanistic investigations. Search terms included “Botulinum Toxin,” “BoNT,” “major depressive disorder,” “bipolar depression,” and “facial feedback.” Results: Some randomized and observational studies would indicate that glabellar BoNT-A injections might lead to significant reductions of depressive symptoms in patients with MDD and TRD. Proposed mechanisms include both peripheral modulation of emotional expression and brain effects, such as reduced amygdala hyperactivity, increased BDNF expression, and enhanced monoaminergic transmission. Preclinical studies confirm that BoNT-A modulates limbic and brainstem circuits, possibly implicated in affective regulation. The few comparative studies suggest therapeutic efficacy comparable to that of SSRIs, with a more rapid onset. Preliminary data also support its application in bipolar depression and comorbid anxiety disorders. Conclusions: The available literature would indicate that BoNT-A might constitute a promising candidate at least as an adjunctive treatment in MDD, although the impact of current findings is limited due to the methodological heterogeneity and the small sample sizes of patients examined. Further large-scale, placebo-controlled trials are warranted to elucidate the mode of action of BoNT-A and to validate or not its clinical effectiveness.