Background: Neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and amyotrophic lateral sclerosis, represent a major global health burden and share convergent pathogenic mechanisms, such as mitochondrial dysfunction, oxidative stress, neuroinflammation, calcium imbalance, and neuronal loss. Despite advances in symptomatic management, effective disease-modifying therapies remain limited. Objectives: This review aims to critically synthesize mechanistic, preclinical, and clinical evidence on α-lipoic acid and biotin as candidate neuroprotective agents in neurodegenerative diseases, with emphasis on shared signaling pathways, therapeutic potential, generally favorable safety profiles, and translational limitations. Methods: A narrative and integrative review was conducted, encompassing mechanistic studies, preclinical experimental models, and clinical trials and observational studies evaluating ALA and biotin in neurodegenerative diseases. The evidence was qualitatively analyzed with attention to biological plausibility, consistency across models, and clinical relevance. Results: ALA and biotin modulate key cellular pathways implicated in neurodegeneration, including mitochondrial metabolism, redox homeostasis, inflammatory signaling, and neurovascular function. Preclinical studies consistently report beneficial effects on mitochondrial efficiency, oxidative stress, and neuroinflammatory markers. In contrast, clinical evidence remains heterogeneous, with more extensive evaluation of biotin in progressive multiple sclerosis and more limited or exploratory findings for ALA across neurodegenerative disorders. Conclusions: ALA and biotin exhibit mechanistic convergence across pathways relevant to neurodegeneration and generally favorable safety profiles. Although current evidence supports their biological plausibility as adjunctive or exploratory therapeutic strategies, clinical outcomes remain inconsistent and appear to be influenced by dosing regimens, disease stage at intervention, and endpoint selection. Well-designed clinical studies are required to define their efficacy, optimal dosing, and disease-specific applicability.

Numerous studies indicate that intrauterine growth restriction (IUGR) can predispose individuals to metabolic syndrome (MetS) in adulthood. Several reports have demonstrated that pharmacological concentrations of biotin have therapeutic effects on MetS. The present study investigated the beneficial effects of prenatal biotin supplementation in a rat model of intrauterine caloric restriction to prevent cardiometabolic risk in adult female offspring fed fructose after weaning. Female rats were exposed to a control (C) diet or global caloric restriction (20%) (GCR), with biotin (GCRB) supplementation (2 mg/kg) during pregnancy. Female offspring were exposed to 20% fructose (F) in drinking water for 16 weeks after weaning (C, C/F, GCR/F, and GCRB/F). The study assessed various metabolic parameters including Lee’s index, body weight, feed conversion ratio, caloric intake, glucose tolerance, insulin resistance, lipid profile, hepatic triglycerides, blood pressure, and arterial vasoconstriction. Results showed that GCR and GCRB dams had reduced weights compared to C dams. Offspring of GCRB/F and GCR/F dams had lower body weight and Lee’s index than C/F offspring. Maternal biotin supplementation in the GCRB/F group significantly mitigated the adverse effects of fructose intake, including hypertriglyceridemia, hypercholesterolemia, hepatic steatosis, glucose and insulin resistance, hypertension, and arterial hyperresponsiveness. This study concludes that prenatal biotin supplementation can protect against cardiometabolic risk in adult female offspring exposed to postnatal fructose, highlighting its potential therapeutic benefits.

Las enfermedades crónicas no transmisibles son la principal causa de muerte en el mundo. Entre ellas, las cardiovasculares ocupan el primer lugar en mortalidad y el principal factor de riesgo es la hipertensión, la cual suele ser asintomática hasta que los efectos perjudiciales se manifiestan. Existe una fuerte relación entre la hipertensión y el riñón, ya que por un lado la hipertensión es el mayor factor de riesgo para la iniciación y progresión de la enfermedad renal y al mismo tiempo la hipertensión es el resultado de la propia enfermedad renal. En esta revisión, se analizaron de manera general diferentes aspectos de la hipertensión arterial, como prevalencia, clasificación, etiología, heredabilidad y relación con enfermedades crónicas no transmisibles y la importancia del riñón en la regulación de la presión arterial; así como la enfermedad renal y su relación con la hipertensión y las consecuenciasdeletéreas para la salud.

Actualmente científicos de todo el mundo centran sus esfuerzos en desarrollar alternativas de reemplazo de tejidos enfermos, que no cumplen satisfactoriamente las funciones orgánicas normales. En este contexto, las técnicas de ingeniería tisular permiten la generación de tejidos ex vivo, con la propiedad de ser incorporados al organismo y reemplazar el tejido dañado o enfermo para incrementar, disminuir o modificar sus funciones mediante injertos autólogos. Estas técnicas permiten actualmente sustituir órganos humanos afectados, a partir de tejidos artificiales que la ingeniería tisular admite generar en el laboratorio. Esto sustituye a los aloinjertos, que a su vez pueden ocasionar rechazo, transmisión de enfermedades e involución del material injertado. Debido a la importancia que desempeñan las células troncales utilizadas para la generación de los tejidos en laboratorio, este trabajo abordará mediante revisión de la literatura los aspectos generales de las células troncales, células progenitoras o mesenquimales, biomateriales y factores de crecimiento.

Information about the paper titled "ADAPTATIONS MADE IN ORTHODONTIC DENTISTRY CLINICS AT MEXICAN UNIVERSITIES DURING THE SARS2-COV-19 PANDEMIC" at IATED Digital Library