Objetivos: Analisar as principais produções da literatura científica brasileira sobre a prevalência e os fatores associados aos transtornos mentais entre estudantes universitários da área da saúde. Fonte de dados: Foi realizada uma revisão narrativa da literatura nas bases de dados Scielo, PubMed e Science Direct, sendo incluídas 15 pesquisas originais sobre o tema. Conclusão: O cuidado em saúde mental durante a graduação, com ênfase na prevenção do adoecimento mental dos estudantes da saúde, perpassa por nuances que exigem dos alunos diversas adaptações. É urgente e necessário o envolvimento das instituições de ensino no desenvolvimento de políticas educacionais e oferta de serviços de suporte terapêutico nesse processo.Palavras-chave: Saúde Mental. Transtornos Mentais. Serviços de Saúde para Estudantes. Depressão. Ansiedade.

The neurology, psychiatry and psychology areas have played a fundamental role in the characterization of cognitive disturbances associated to dementia disorders, which has contributed to the improvement of diagnostic and therapeutic procedures. Semantic dementia is a subgenre of frontotemporal dementia, consists in a syndrome of primary progressive aphasia characterized by the loss of semantic knowledge, with the preservation of other cognitive functions, such as visual memory, visuospatial capacity, and executive abilities. Thus, the relevance of this study consists in thoroughly analyzing the main alterations in which concerns the behavior of semantic dementia, aiming to know more about this rare subtype of frontotemporal dementia, so that in the future its clinical manifestations, diagnosis and treatment are better elucidated. A narrative literature review was executed in the Medline database (PubMed), from 2010 to 2022, about behavioral alterations in semantic dementia. The present literature review article demonstrates the current comprehension about cognitive, behavioral, and functional alterations as a semantic dementia consequence, besides providing relevant information to prioritize the therapeutic offered to patients that have such a condition. Furthermore, more studies addressing this subject are paramount since the existing studies are still not sufficient to completely elucidate the behavioral changes in semantic dementia.

The neurology, psychiatry and psychology areas have played a fundamental role in the characterization of cognitive disturbances associated to dementia disorders, which has contributed to the improvement of diagnostic and therapeutic procedures. Semantic dementia is a subgenre of frontotemporal dementia, consists in a syndrome of primary progressive aphasia characterized by the loss of semantic knowledge, with the preservation of other cognitive functions, such as visual memory, visuospatial capacity, and executive abilities. Thus, the relevance of this study consists in thoroughly analyzing the main alterations in which concerns the behavior of semantic dementia, aiming to know more about this rare subtype of frontotemporal dementia, so that in the future its clinical manifestations, diagnosis and treatment are better elucidated. A narrative literature review was executed in the Medline database (PubMed), from 2010 to 2022, about behavioral alterations in semantic dementia. The present literature review article demonstrates the current comprehension about cognitive, behavioral, and functional alterations as a semantic dementia consequence, besides providing relevant information to prioritize the therapeutic offered to patients that have such a condition. Furthermore, more studies addressing this subject are paramount since the existing studies are still not sufficient to completely elucidate the behavioral changes in semantic dementia.

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized primarily by motor symptoms, including bradykinesia, rigidity, and resting tremor, and is frequently accompanied by a spectrum of non-motor manifestations suchThe Genetic Landscape of Parkinson's Disease: Current Advances and Persistent GapsThe genetic architecture of PD encompasses both rare, high-penetration variants in genes such as SNCA, LRRK2, PINK1, PRKN, and DJ-1, and common, low-effect polymorphisms identified through GWAS approaches (Blauwendraat et al., 2020). While pathogenic mutations in LRRK2 and GBA account for a fraction of familial and sporadic PD cases, many risk-associated variants lie within noncoding regions, modulating gene expression through subtle regulatory mechanisms (Ito;Utsunomiya-Tate, 2023).Recent studies reinforce the importance of SNCA polymorphisms, especially rs356165, rs356219, and rs11931074, across populations, although their effect sizes differ by ancestry (Mohammadi et al., 2025). Such variability likely reflects differences in linkage disequilibrium structure, chromatin organization, and DNA methylation landscapes, suggesting that epigenetic regulation of SNCA may be ancestry-dependent. Despite these findings, most data originate from European cohorts, whose data dominate GWAS repositories and meta-analyses. Consequently, the transferability of these results to admixed genomes, such as those found in Latin American, African, or South Asian populations, remains highly uncertain (Saffie Awad et al., 2024;Saffie Awad et al., 2025). Santos-Lobato et al. (2021) highlighted this paradox in their review. For example, in Brazil, one of the world's most genetically diverse nations (Nunes et al., 2025), only 3.2% of PD patients screened had identifiable monogenic mutations, and population admixture was rarely analyzed (Santos-Lobato et al., 2021). Countries with the richest ancestral diversity thus contribute the least to genetic discovery, while results from homogeneous European samples are often generalized to the entire human population. This imbalance undermines the promise of precision medicine in PD. PRSs derived from European datasets commonly lack reproducibility in non-Europeans and in admixed populations. For instance, LRRK2 p.G2019S, prevalent among Ashkenazi Jews and North African Arabs, exhibits low frequency in East Asians but displays variable penetrance in Latin American cohorts. Similarly, GBA variants, critical risk modifiers, show heterogeneous effects across ancestries, influenced by background haplotypes and local selective pressures (Claudino dos Santos et al., 2024).Populations such as those in Brazil, Colombia, Mexico, and South Africa represent unique genetic mosaics that can shed light on novel biological pathways and protective mechanisms. The persistent underrepresentation of these groups perpetuates misclassification of variants and diagnostic uncertainty. Understanding allele frequencies, linkage patterns, and gene-environment interactions within these populations could refine pathogenicity assessments and enable more accurate genetic counseling. Moreover, epigenetic plasticity within SNCA intronic regions, varying by ancestry, may influence transcriptional dynamics and disease onset, further demonstrating that diversity is not optional but essential for comprehensive genomic interpretation (Sharma et al., 2019).A compelling illustration of the consequences of underrepresentation comes from another disease, transthyretin amyloidosis (ATTR) (Bharaj et al., 2025). As discussed by Bharaj et al. (2025), the TTR V122I variant, carried by approximately 3.4% of African Americans, was long neglected in cardiogenetic research due to Eurocentric sampling. Only when African ancestry populations were investigated did the variant's pathogenic role in heart failure become evident, ultimately leading to the development of targeted therapies such as Tafamidis. This case demonstrates how inclusion can drive therapeutic innovation when diversity is integrated into discovery pipelines: new biological pathways emerge, and medical inequities begin to narrow. We see that a similar transformation is needed in the context of PD (Bharaj et al., 2025).Expanding genetic studies to underrepresented and admixed populations could reveal ancestry-specific modulators of α-synuclein aggregation, lysosomal function, or mitochondrial dynamics, all of which are central to neurodegeneration. Countries with mixed ancestries serve as natural laboratories for exploring gene-environment interactions. For example, the Brazilian population's heterogeneous admixture, predominantly European in the South, mixed African and Indigenous in the North and Northeast, mirrors global genetic variation and offers a fertile ground for trans-ancestral mapping. Yet, as reported by Santos-Lobato et al. (2021), fewer than 100 Brazilian PD patients have been genetically characterized to date.Incorporating such populations would refine PRS calibration and variant interpretation. A variant labeled as "pathogenic" in a European cohort may be benign, or even protective, in an admixed genome. Without ancestry-adjusted databases, clinical misinterpretations are inevitable, perpetuating inequities in diagnosis and access to treatment. Thus, expanding PD genomics to include underrepresented populations is not merely an act of inclusion, it is a scientific necessity for the validity and global applicability of genetic medicine.The lack of diversity in PD genetic research remains a significant barrier to advancing the field (Schumacher-Schuh et al., 2022). More than 75% of participants in PD GWAS are of European ancestry, while fewer than 4% represent African, Latin American, or Asian, other than Chinese, ancestry. This imbalance has deep ethical and scientific implications, influencing not only the interpretation of genetic risk but also how diagnostic and therapeutic tools are developed and implemented...

Background/Objectives: Fibromyalgia (FM) is a nociplastic pain syndrome characterized by chronic widespread pain, fatigue, sleep disturbance, cognitive dysfunction, and heightened sensitivity to somatic and environmental stimuli. Depressive symptoms and major depressive disorder (MDD) frequently co-occur with FM and are associated with greater disability, pain catastrophizing, sleep disruption, and poorer treatment response. Although pharmacological treatments can reduce symptoms in some patients, many individuals experience persistent functional and affective burden, highlighting the need for mechanism-based adjunctive strategies. Mindfulness-based interventions (MBIs), particularly mindfulness-based stress reduction (MBSR), have shown promise for improving functional impact, pain catastrophizing, perceived stress, depressive symptoms, sleep-related burden, and quality of life in FM. However, the effects of MBIs on pain intensity and biomarkers are less consistent. Methods: This narrative mechanistic review develops a hypothesis-generating multisystem neurobehavioral framework to explain how MBIs may influence pain–mood coupling in FM with depressive symptom burden. We define pain–mood recalibration as a reduction in the extent to which pain intensity, bodily vigilance, and interoceptive threat appraisal automatically drive depressive symptoms, rumination, avoidance, and functional disengagement. Results: Fibromyalgia-specific evidence most strongly supports cognitive–emotional mechanisms, including reduced catastrophizing, psychological inflexibility, rumination, perceived stress, and avoidance. Interoceptive, neural-network, autonomic, immune-inflammatory, and sleep-fatigue-behavioral pathways remain exploratory and require prospective mediation and moderation testing. Conclusions: Future trials should prioritize active controls, ecological momentary assessment, longitudinal biomarkers, neuroimaging, interoceptive tasks, and formal mediation/moderation models to determine which patients benefit, through which mechanisms, and under what biological and psychological conditions.

Background/Objectives: Gabapentin is a first-line treatment for neuropathic pain, classically understood to reduce neuronal excitability through binding to the alpha-2-delta-1 (α2δ-1) subunit of voltage-gated calcium channels. However, this neuron-centric model does not fully explain its variable clinical efficacy across pain syndromes. In parallel, chronic pain is increasingly conceptualized as involving neuron–glia–immune interactions, in which microglial activation, astrocytic signaling, and inflammatory mediators may contribute to central sensitization. Methods: A structured narrative review was conducted using PubMed, Web of Science, and Google Scholar for articles available through December 2025. The search focused on gabapentin/gabapentinoids, chronic and neuropathic pain, α2δ-1 mechanisms, neuron–glia interactions, neuroinflammation, central and peripheral sensitization, nociplastic pain, cytokine/chemokine signaling, and neuroimmune modulation. Basic science studies, animal models, translational studies, clinical trials, reviews, meta-analyses, and guidelines were narratively synthesized. Results: Preclinical evidence indicates that gabapentin reduces neuronal hyperexcitability and may secondarily attenuate neuron-to-glia signaling, glial activation, and cytokine- and chemokine-related pathways. However, these neuroimmune effects remain predominantly preclinical, model-dependent, and incompletely validated in humans. Clinical evidence supports gabapentin for selected neuropathic pain conditions, but human studies rarely evaluate glial activation, cytokine signaling, or neuroimmune biomarkers. Conclusions: Gabapentin remains best understood as a neuronal α2δ-1 modulator. Although preclinical and translational evidence suggests biologically plausible secondary effects on neuroimmune signaling, these mechanisms have not been validated as biomarkers or prescribing targets in humans. The conceptual framework presented in this review supports mechanism-informed clinical reasoning and individualized pain management but should not be interpreted as a biomarker-guided prescribing algorithm. Clinically, gabapentin should be prescribed selectively for patients with neuropathic or sensitized pain features, using predefined functional goals, appropriate renal dose adjustment, careful safety monitoring, and discontinuation when meaningful benefit is not achieved.