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Rosacea is a chronic dermatological condition that currently lacks a clear treatment approach due to an uncomprehensive knowledge of its pathogenesis. The main obstacle lies in understanding its etiology and the mode of action of the different drugs used. This study aims to clarify these aspects by employing drug repositioning. Using an in silico approach, we performed a transcriptomic analysis comparing samples from individuals with diverse types of rosacea to those from healthy controls to identify genes deregulated in this disease. Subsequently, we realized molecular docking and molecular dynamics studies to assess the binding affinity of drugs currently used to treat rosacea and drugs that target proteins interacting with, and thus affecting, proteins deregulated in rosacea. Our findings revealed that the downregulation of SKAP2 and upregulation of S100A7A in rosacea, could be involved in the pathogenesis of the disease. Furthermore, considering the drugs currently used for rosacea management, we demonstrated stable interactions between isotretinoin and BFH772 with SKAP2, and permethrin and PAC-14028 with S100A7A. Similarly, considering drugs targeting SKAP2 and S100A7A interactome proteins, we found that pitavastatin and dasatinib exert stable interactions with SKAP2, and lovastatin and tirbanibulin with S100A7A. In addition, we determine that the types of bonds involved in the interactions were different in SKAP2 from S100A7A. The drug-SKAP2 interactions are hydrogen bonds, whereas the drug-S100A7A interactions are of the hydrophobic type. In conclusion, our study provides evidence for the possible contribution of SKAP2 and S100A7A to rosacea pathology. Furthermore, it provides significant information on the molecular interactions between drugs and these proteins, highlighting the importance of considering structural features and binding interactions in the design of targeted therapies for skin disorders such as rosacea.

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BACKGROUND: Glycogen storage disease type Ia (GSD-Ia) is one of the most common hepatic GSD. Its treatment mainly consists of a diet including a high intake of slow-digestion carbohydrates such as raw cornstarch and the restriction of simple sugars. This enables the maintenance of euglycemia and prevents secondary metabolic disorders. Starch is a glucose polymer formed by amylose and amylopectin, which can be obtained from distinct sources. Although uncooked cornstarch has been successfully used in the treatment of GSD-Ia, it can lead to hyperglycemia and weight gain. in vitro andin vivo tests indicated that sweet manioc starch can be potentially used in the treatment of GSD-Ia. RESULTS: The moisture analysis revealed a variation from 10.3 to 12.8% in the sweet manioc starch samples, whereas the moisture content of uncooked cornstarch ranged from 7.3 to 11.1%. Quantifiable sugar was detected in 3/5 samples of sweet manioc starch and 1/3 samples of uncooked cornstarch. Notably, this uncooked cornstarch brand is widely employed in GSD-Ia treatment in Brazil. Products B and E had higher values of amylopectin and undetectable levels of sugars. A clinical trial is warranted to compare samples F and G and determine the impact of sugar trace in the same dietary source of starch. CONCLUSIONS: Collectively, the results demonstrated possible therapeutic alternatives for GSD-Ia in addition to traditional uncooked cornstarch.

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Introduction: Gastric cancer is one of the most prevalent types of cancer worldwide. The World Health Organization (WHO), the International Agency for Research on Cancer (IARC), and the Global Cancer Statistics (GLOBOCAN) reported an age standardized global incidence rate of 9.2 per 100,000 individuals for gastric cancer in 2022, with a mortality rate of 6.1. Despite considerable progress in precision oncology through the efforts of international consortia, understanding the genomic features and their influence on the effectiveness of anti-cancer treatments across diverse ethnic groups remains essential. Methods: Our study aimed to address this need by conducting integrated in silico analyses to identify actionable genomic alterations in gastric cancer driver genes, assess their impact using deleteriousness scores, and determine allele frequencies across nine global populations: European Finnish, European non-Finnish, Latino, East Asian, South Asian, African, Middle Eastern, Ashkenazi Jewish, and Amish. Furthermore, our goal was to prioritize targeted therapeutic strategies based on pharmacogenomics clinical guidelines, in silico drug prescriptions, and clinical trial data. Results: Our comprehensive analysis examined 275,634 variants within 60 gastric cancer driver genes from 730,947 exome sequences and 76,215 whole-genome sequences from unrelated individuals, identifying 13,542 annotated and predicted oncogenic variants. We prioritized the most prevalent and deleterious oncogenic variants for subsequent pharmacogenomics testing. Additionally, we discovered actionable genomic alterations in the ARID1A, ATM, BCOR, ERBB2, ERBB3, CDKN2A, KIT, PIK3CA, PTEN, NTRK3, TP53, and CDKN2A genes that could enhance the efficacy of anti-cancer therapies, as suggested by in silico drug prescription analyses, reviews of current pharmacogenomics clinical guidelines, and evaluations of phase III and IV clinical trials targeting gastric cancer driver proteins. Discussion: These findings underline the urgency of consolidating efforts to devise effective prevention measures, invest in genomic profiling for underrepresented populations, and ensure the inclusion of ethnic minorities in future clinical trials and cancer research in developed countries.

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Dengue virus (DENV) is a major global health concern, causing millions of infections annually. Understanding the cellular response to DENV infection is crucial for developing effective therapies. This study provides an in-depth analysis of the cellular response to Dengue virus (DENV) infection, with a specific focus on the interplay between microRNAs (miRNAs), apoptosis, and viral load across different DENV serotypes. Utilizing a variety of cell lines infected with four DENV serotypes, the research methodically quantifies viral load, and the expression levels of miRNA-15, miRNA-16, and BCL2 protein, alongside measuring apoptosis markers. Methodologically, the study employs quantitative PCR for viral load and miRNA expression analysis, and Western blot for apoptosis and BCL2 detection, with a statistical framework that includes ANOVA and correlation analysis to discern significant differences and relationships. The findings reveal that despite similar viral loads across DENV serotypes, DENV-2 exhibits a marginally higher load. A notable upregulation of miRNA-15 and miRNA-16 correlates positively with increased viral load, suggesting their potential role in modulating viral replication. Concurrently, a marked activation of caspases 3 and 7, along with changes in BCL2 protein levels, underscores the role of apoptosis in the cellular response to DENV infection. Conclusively, the study enhances the understanding of miRNA involvement in DENV pathogenesis, highlighting miRNA-15 and miRNA-16 as potential regulatory agents in viral replication and apoptosis. These findings pave the way for further exploration into miRNA-based therapeutic strategies against DENV infection.

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Acute Lymphoblastic Leukemia (ALL) is the predominant hematological malignancy in pediatric populations, originating from B- or T-cell precursors within the bone marrow. The disease exhibits a high degree of heterogeneity, both at the molecular level and in terms of clinical presentation. A complex interplay between inherited and acquired genetic alterations contributes to disease pathogenesis, often resulting in the disruption of cellular functions integral to the leukemogenic process. The advent of CRISPR/Cas9 as a gene editing tool has revolutionized biological research, underscoring its potential to modify specific genomic loci implicated in cancer. Enhanced understanding of molecular alterations in ALL has facilitated significant advancements in therapeutic strategies. In this review, we scrutinize the application of CRISPR/Cas9 as a tool for identifying genetic targets to improve therapy, circumvent drug resistance, and facilitate CAR-T cell-based immunotherapy. Additionally, we discuss the challenges and future prospects of CRISPR/Cas9 applications in ALL.

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The COVID-19 pandemic generated, in addition to severe symptoms, hospitalizations and deaths worldwide, as well as stress from the fear of the disease and social uncertainties, from restriction measures and social isolation. Stress from social isolation impacts mental health, aggravating existing conditions and triggering neuropsychiatric symptoms in individuals with biopsychosocial vulnerability. During and immediately after the period of social restriction imposed by the pandemic, the scientific community carried out several research protocols. These revealed results that relevantly demonstrate the harmful effect of the stress induced by the pandemic situation. This narrative review reports and discusses research results demonstrating impairments in psychiatric disorders such as autism spectrum disorder, dementia, eating disorders, schizophrenia, anxiety, and depression. In this sense, the community has identified a significant negative influence of social isolation on the mental health of individuals through the modification of individual routines and the absence of social interactions. Moreover, the community identified perceived differences related to the impacts on men and women. In addition to studies showing the effect of social isolation on disorders, an evaluation of protocols with some possible therapeutic intervention strategies during times of social restriction was developed.

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Visual impairment and blindness are a growing public health problem as they reduce the life quality of millions of people. The management and treatment of these diseases represent scientific and therapeutic challenges because different cellular and molecular actors involved in the pathophysiology are still being identified. Visual system components, particularly retinal cells, are extremely sensitive to genetic or metabolic alterations, and immune responses activated by local insults contribute to biological events, culminating in vision loss and irreversible blindness. Several ocular diseases are linked to retinal cell loss, and some of them, such as retinitis pigmentosa, age-related macular degeneration, glaucoma, and diabetic retinopathy, are characterized by pathophysiological hallmarks that represent possibilities to study and develop novel treatments for retinal cell degeneration. Here, we present a compilation of revisited information on retinal degeneration, including pathophysiological and molecular features and biochemical hallmarks, and possible research directions for novel treatments to assist as a guide for innovative research. The knowledge expansion upon the mechanistic bases of the pathobiology of eye diseases, including information on complex interactions of genetic predisposition, chronic inflammation, and environmental and aging-related factors, will prompt the identification of new therapeutic strategies.

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The advancement of knowledge in pathophysiology and underlying etiologies of gastroesophageal reflux disease (GERD) has allowed the development of the concept of disease beyond the acidity of reflux. The variability in the symptom presentation and the response to treatment cannot be attributed only to reflux composition, since esophageal factors, such as structural, mechanical, biochemical, and physiological aspects, play an important role. The proposed personalized approach to GERD uses a stepwise approach that optimizes performance and phenotypic outcome while minimizing invasiveness, risk, and cost. Throughout the staggered approach to determine the GERD phenotype, clinicians may choose to stop further testing and continue treatment if available information identifies a different GERD phenotype. Since not all phenotypes GERD are the same and not all treatments are appropriate for all patients, therapeutic strategies must be personalized according to their phenotype.

El avance del conocimiento sobre la fisiopatología y la etiología subyacentes a la enfermedad por reflujo gastroesofágico (ERGE) ha permitido que el desarrollo de esta se extienda más allá de la acidez del reflujo. La variabilidad en la presentación de los síntomas y la respuesta al tratamiento no se puede atribuir solo a la composición del reflujo, ya que factores esofágicos, como aspectos estructurales, mecánicos, bioquímicos y fisiológicos, desempeñan un papel importante. El enfoque personalizado propuesto para la ERGE utiliza un método gradual que optimiza el rendimiento y el resultado fenotípico, y minimiza la invasividad, el riesgo y el costo. A lo largo del método escalonado para determinar el fenotipo de la ERGE, los médicos pueden optar por detener las pruebas adicionales y continuar con el tratamiento si la información disponible identifica un fenotipo de ERGE distinto. Dado que la ERGE no es la misma y no todos los tratamientos disponibles para controlarla son apropiados para todos los pacientes, las estrategias terapéuticas deben personalizarse de acuerdo con su fenotipo.

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Neurodegenerative diseases (NDDs) are characterized by the progressive degeneration and/or loss of neurons belonging to the central nervous system, and represent one of the major global health issues. Therefore, a number of immunotherapeutic approaches targeting the non-functional or toxic proteins that induce neurodegeneration in NDDs have been designed in the last decades. In this context, due to unprecedented advances in genetic engineering techniques and molecular farming technology, pioneering plant-based immunogenic antigen expression systems have been developed aiming to offer reliable alternatives to deal with important NDDs, including Alzheimer's disease, Parkinson's disease, and multiple sclerosis. Diverse reports have evidenced that plant-made vaccines trigger significant immune responses in model animals, supported by the production of antibodies against the aberrant proteins expressed in the aforementioned NDDs. Moreover, these immunogenic tools have various advantages that make them a viable alternative for preventing and treating NDDs, such as high scalability, no risk of contamination with human pathogens, cold chain free production, and lower production costs. Hence, this article presents an overview of the current progress on plant-manufactured vaccines for NDDs and discusses its future prospects.

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Lung cancer is one of the most frequent tumors that metastasize to the brain. Brain metastasis (BM) is common in advanced cases, being the major cause of patient morbidity and mortality. BMs are thought to arise via the seeding of circulating tumor cells into the brain microvasculature. In brain tissue, the interaction with immune cells promotes a microenvironment favorable to the growth of cancer cells. Despite multimodal treatments and advances in systemic therapies, lung cancer patients still have poor prognoses. Therefore, there is an urgent need to identify the molecular drivers of BM and clinically applicable biomarkers in order to improve disease outcomes and patient survival. The goal of this review is to summarize the current state of knowledge on the mechanisms of the metastatic spread of lung cancer to the brain and how the metastatic spread is influenced by the brain microenvironment, and to elucidate the molecular determinants of brain metastasis regarding the role of genomic and transcriptomic changes, including coding and non-coding RNAs. We also present an overview of the current therapeutics and novel treatment strategies for patients diagnosed with BM from NSCLC.

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Visual impairment and blindness are a growing public health problem as they reduce the life quality of millions of people. The management and treatment of these diseases represent scientific and therapeutic challenges because different cellular and molecular actors involved in the pathophysiology are still being identified. Visual system components, particularly retinal cells, are extremely sensitive to genetic or metabolic alterations, and immune responses activated by local insults contribute to biological events, culminating in vision loss and irreversible blindness. Several ocular diseases are linked to retinal cell loss, and some of them, such as retinitis pigmentosa, age-related macular degeneration, glaucoma, and diabetic retinopathy, are characterized by pathophysiological hallmarks that represent possibilities to study and develop novel treatments for retinal cell degeneration. Here, we present a compilation of revisited information on retinal degeneration, including pathophysiological and molecular features and biochemical hallmarks, and possible research directions for novel treatments to assist as a guide for innovative research. The knowledge expansion upon the mechanistic bases of the pathobiology of eye diseases, including information on complex interactions of genetic predisposition, chronic inflammation, and environmental and aging-related factors, will prompt the identification of new therapeutic strategies.

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The raising prevalence of obesity is associated with an increased risk for cardiovascular diseases (CVDs), particularly coronary artery disease (CAD), and heart failure, including atrial fibrillation, ventricular arrhythmias and sudden death. Obesity contributes directly to incident cardiovascular risk factors, including hyperglycemia or diabetes, dyslipidemia, and hypertension, which are involved in atherosclerosis, including structural and functional cardiac alterations, which lead to cardiac dysfunction. CVDs are the main cause of morbidity and mortality worldwide. In obesity, visceral and epicardial adipose tissue generate inflammatory cytokines and reactive oxygen species (ROS), which induce oxidative stress and contribute to the pathogenesis of CVDs. Nuclear factor erythroid 2-related factor 2 (NRF2; encoded by Nfe2l2 gene) protects against oxidative stress and electrophilic stress. NRF2 participates in the regulation of cell inflammatory responses and lipid metabolism, including the expression of over 1000 genes in the cell under normal and stressed environments. NRF2 is downregulated in diabetes, hypertension, and inflammation. Nfe2l2 knockout mice develop structural and functional cardiac alterations, and NRF2 deficiency in macrophages increases atherosclerosis. Given the endothelial and cardiac protective effects of NRF2 in experimental models, its activation using pharmacological or natural products is a promising therapeutic approach for obesity and CVDs. This review provides a comprehensive summary of the current knowledge on the role of NRF2 in obesity-associated cardiovascular risk factors.

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Hepatocellular carcinoma (HCC) is the most common primary liver cancer and is the sixth most frequent cancer in the world, being the third cause of cancer-related deaths. Nonalcoholic steatohepatitis (NASH) is characterized by fatty infiltration, oxidative stress and necroinflammation of the liver, with or without fibrosis, which can progress to advanced liver fibrosis, cirrhosis and HCC. Obesity, metabolic syndrome, insulin resistance, and diabetes exacerbates the course of NASH, which elevate the risk of HCC. The growing prevalence of obesity are related with increasing incidence of NASH, which may play a growing role in HCC epidemiology worldwide. In addition, HCC initiation and progression is driven by reprogramming of metabolism, which indicates growing appreciation of metabolism in the pathogenesis of this disease. Although no specific preventive pharmacological treatments have recommended for NASH, dietary restriction and exercise are recommended. This review focuses on the molecular connections between HCC and NASH, including genetic and risk factors, highlighting the metabolic reprogramming and aberrant epigenetic alterations in the development of HCC in NASH. Current therapeutic aspects of NASH/HCC are also reviewed.

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As the development of new drugs for Chagas disease is not a priority due to its neglected disease status, an option for increasing treatment adherence is to explore alternative treatment regimens, which may decrease the incidence of side effects. Therefore, we evaluated the efficacy of different therapeutic schemes with benznidazole (BNZ) on the acute and chronic phases of the disease, using mice infected with strains that have different BNZ susceptibilities. Our results show that the groups of animals infected by VL-10 strain, when treated in the chronic phase with a lower dose of BNZ for a longer period of time (40 mg/kg/day for 40 days) presented better treatment efficacy than with the standard protocol (100 mg/kg/day for 20 days) although the best result in the treatment of the animals infected by the VL-10 strain was with100 mg/kg/day for 40 days. In the acute infection by the Y and VL-10 strains of T. cruzi, the treatment with a standard dose, but with a longer time of treatment (100 mg/kg/day for 40 days) presented the best results. Given these data, our results indicate that for BNZ, the theory of dose and time proportionality does not apply to the phases of infection.

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A review of recent animal models of Huntington's disease showed many microRNAs had altered expression levels in the striatum and cerebral cortex, and which were mostly downregulated. Among the altered microRNAs were miR-9/9*, miR-29b, miR-124a, miR-132, miR-128, miR-139, miR-122, miR-138, miR-23b, miR-135b, miR-181 (all downregulated) and miR-448 (upregulated), and similar changes had been previously found in Huntington's disease patients. In the animal cell studies, the altered microRNAs included miR-9, miR-9*, miR-135b, miR-222 (all downregulated) and miR-214 (upregulated). In the animal models, overexpression of miR-155 and miR-196a caused a decrease in mutant huntingtin mRNA and protein level, lowered the mutant huntingtin aggregates in striatum and cortex, and improved performance in behavioral tests. Improved performance in behavioral tests also occurred with overexpression of miR-132 and miR-124. In the animal cell models, overexpression of miR-22 increased the viability of rat primary cortical and striatal neurons infected with mutant huntingtin and decreased huntingtin -enriched foci of ≥ 2 µm. Also, overexpression of miR-22 enhanced the survival of rat primary striatal neurons treated with 3-nitropropionic acid. Exogenous expression of miR-214, miR-146a, miR-150, and miR-125b decreased endogenous expression of huntingtin mRNA and protein in HdhQ111/HdhQ111 cells. Further studies with animal models of Huntington's disease are warranted to validate these findings and identify specific microRNAs whose overexpression inhibits the production of mutant huntingtin protein and other harmful processes and may provide a more effective means of treating Huntington's disease in patients and slowing its progression.

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Glioblastoma (GBM) is the highest-grade form of glioma, as well as one of the most aggressive types of cancer, exhibiting rapid cellular growth and highly invasive behavior. Despite significant advances in diagnosis and therapy in recent decades, the outcomes for high-grade gliomas (WHO grades III-IV) remain unfavorable, with a median overall survival time of 15-18 months. The concept of cancer stem cells (CSCs) has emerged and provided new insight into GBM resistance and management. CSCs can self-renew and initiate tumor growth and are also responsible for tumor cell heterogeneity and the induction of systemic immunosuppression. The idea that GBM resistance could be dependent on innate differences in the sensitivity of clonogenic glial stem cells (GSCs) to chemotherapeutic drugs/radiation prompted the scientific community to rethink the understanding of GBM growth and therapies directed at eliminating these cells or modulating their stemness. This review aims to describe major intrinsic and extrinsic mechanisms that mediate chemoradioresistant GSCs and therapies based on antineoplastic agents from natural sources, derivatives, and synthetics used alone or in synergistic combination with conventional treatment. We will also address ongoing clinical trials focused on these promising targets. Although the development of effective therapy for GBM remains a major challenge in molecular oncology, GSC knowledge can offer new directions for a promising future.

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Cancer constitutes the second leading cause of death globally and is considered to have been responsible for an estimated 9.6 million fatalities in 2018. Although treatments against gastrointestinal tumors have recently advanced, those interventions can only be applied to a minority of patients at the time of diagnosis. Therefore, new therapeutic options are necessary for advanced stages of the disease. Glycosylation of antitumor agents, has been found to improve pharmacokinetic parameters, reduce side effects, and expand drug half-life in comparison with the parent compounds. In addition, glycosylation of therapeutic agents has been proven to be an effective strategy for their targeting tumor tissue, thereby reducing the doses of the glycodrugs administered to patients. This review focusses on the effect of the targeting properties of glycosylated antitumor agents on gastrointestinal tumors.

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Gait disorders may be associated with cognitive impairment, and slow speed predicts cognitive impairment and dementia. OBJECTIVE: To investigate the relationships between cognitive function and gait performance in patients with Parkinson's disease (PD) who attended a hospital neurorehabilitation program. METHODS: Descriptive and inferential statistics (Pearson's correlation) were used for data analysis. The cognitive functions were evaluated through Digit Span, Mental Control, Trail Making Test, Phonemic Verbal Fluency Task, and Addenbrooke's Cognitive Examination III. The motor function was assessed through 10-meter walk test, Mini BESTest and Timed Up and Go Test. RESULTS: A total of 65 patients were included in this study. Of these, 66.15% were males, mean age was 61.14 (8.39) years, mean educational was 12 (8) years, disease progression time was 5.45 (4.37) years. 64.61% were in stages I and II of the Hoehn and Yahr stage. The correlation analyses showed that balance skills are significantly correlated with the ability to switch attention between two tasks and visuospatial function. The function mobility showed a significant correlation with cognitive tests. CONCLUSION: Data suggest the importance of the aspects of switch attention and mental flexibility in gait, evidencing the greater difficulty for double tasks.

Alterações na marcha podem estar associadas ao comprometimento cognitivo, e a velocidade lenta prediz comprometimento cognitivo e demência. Objetivo: Investigar as relações entre a capacidade cognitiva e o desempenho da marcha em pacientes com doença de Parkinson (DP) que participaram de um programa de neurorreabilitação hospitalar. Métodos: A estatística descritiva e inferencial (correlação de Pearson) foi utilizada para análise dos dados. As funções cognitivas foram avaliadas por meio do Teste de Extensão de Dígitos, Controle Mental, Teste de Trilha, Tarefa de Fluência Verbal Fonêmica, Exame Cognitivo de Addenbrooke III. A função motora foi avaliada através do teste de caminhada de 10 metros, Mini BESTest e Timed Up and Go Test. Resultados: Um total de 65 pacientes foi incluído neste estudo. Destes, 66,15% eram do sexo masculino, com média de idade de 61,14 (8,39) anos, com escolaridade média de 12 (8) anos, tempo de evolução da doença de 5,45 (4,37) anos. 64,61% estavam nos estágios I e II do estágio Hoehn e Yahr. As análises de correlação mostraram que as habilidades de equilíbrio estão significativamente correlacionadas com a capacidade de alternar a atenção entre duas tarefas e a função visuoespacial. A função mobilidade apresentou correlação significativa com os testes cognitivos. Conclusão: Os dados sugerem a importância dos aspectos de troca de atenção e flexibilidade mental na marcha, evidenciando a maior dificuldade para tarefas duplas.

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ABSTRACT Gait disorders may be associated with cognitive impairment, and slow speed predicts cognitive impairment and dementia. Objective: To investigate the relationships between cognitive function and gait performance in patients with Parkinson's disease (PD) who attended a hospital neurorehabilitation program. Methods: Descriptive and inferential statistics (Pearson's correlation) were used for data analysis. The cognitive functions were evaluated through Digit Span, Mental Control, Trail Making Test, Phonemic Verbal Fluency Task, and Addenbrooke's Cognitive Examination III. The motor function was assessed through 10-meter walk test, Mini BESTest and Timed Up and Go Test. Results: A total of 65 patients were included in this study. Of these, 66.15% were males, mean age was 61.14 (8.39) years, mean educational was 12 (8) years, disease progression time was 5.45 (4.37) years. 64.61% were in stages I and II of the Hoehn and Yahr stage. The correlation analyses showed that balance skills are significantly correlated with the ability to switch attention between two tasks and visuospatial function. The function mobility showed a significant correlation with cognitive tests. Conclusion: Data suggest the importance of the aspects of switch attention and mental flexibility in gait, evidencing the greater difficulty for double tasks.

RESUMO Alterações na marcha podem estar associadas ao comprometimento cognitivo, e a velocidade lenta prediz comprometimento cognitivo e demência. Objetivo: Investigar as relações entre a capacidade cognitiva e o desempenho da marcha em pacientes com doença de Parkinson (DP) que participaram de um programa de neurorreabilitação hospitalar. Métodos: A estatística descritiva e inferencial (correlação de Pearson) foi utilizada para análise dos dados. As funções cognitivas foram avaliadas por meio do Teste de Extensão de Dígitos, Controle Mental, Teste de Trilha, Tarefa de Fluência Verbal Fonêmica, Exame Cognitivo de Addenbrooke III. A função motora foi avaliada através do teste de caminhada de 10 metros, Mini BESTest e Timed Up and Go Test. Resultados: Um total de 65 pacientes foi incluído neste estudo. Destes, 66,15% eram do sexo masculino, com média de idade de 61,14 (8,39) anos, com escolaridade média de 12 (8) anos, tempo de evolução da doença de 5,45 (4,37) anos. 64,61% estavam nos estágios I e II do estágio Hoehn e Yahr. As análises de correlação mostraram que as habilidades de equilíbrio estão significativamente correlacionadas com a capacidade de alternar a atenção entre duas tarefas e a função visuoespacial. A função mobilidade apresentou correlação significativa com os testes cognitivos. Conclusão: Os dados sugerem a importância dos aspectos de troca de atenção e flexibilidade mental na marcha, evidenciando a maior dificuldade para tarefas duplas.

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BACKGROUND: Kidney diseases are a public health problem worldwide. Available therapies include function replacement by dialysis or transplant, which are associated with a high morbidity and mortality. Likewise, none of these treatments compensate all kidney functions. There is a great concern in developing more effective therapies with the ability to replace the wide range of renal functions, so that, new studies on developing therapeutic strategies have focused on regenerative medicine. OBJECTIVE: The aim of this paper is to review the new advances in regenerative medicine for renal failure treatment. RESULTS: Regenerative medicine comprises two therapeutic strategies: cell therapy and tissue engineering. Cell therapy techniques depend on cell and tissue cultures, with the aim to replace morphological structures, tissues, and functions. The main strategic strength of cell therapy in renal failure is the incorporation of additional cells in a damaged kidney, for which purpose different kind of Stem Cells (SCs) have been used such as Embryonic SCs, induced Pluripotent SCs, Multipotent SCs, Renal SCs, or drugs that increase survival and mobilization of SCs. Tissue engineering complements cell therapy combining techniques of biological sciences and engineering to create structures and devices as scaffolds, matrices or 3D biocompatible materials. CONCLUSION: Even though there is a significant advance in regenerative medicine strategies, we are far from using any of its techniques on health institutions, due to it is necessary to evaluate side effects, biodistribution, dosage, type of administration, vehicle of cell therapy, as well as the evaluation of response time and long-term studies, among other studies.

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