Pub Date : 2025-10-01DOI: 10.1016/j.neuarg.2025.08.001
Angela Francesca Espinoza Baigorria , Elías Cabanillas Mejía , Carlos Zavaleta-Corvera , Maria Isabel De la Cruz Davila , Jose Caballero-Alvarado
Introduction
There is evidence that calcium plays an important role in the pathogenesis of ischemic cerebrovascular accident (CVA), relating to the extent of ischemia and, therefore, to the patient's prognosis. This study aimed to determine if hypocalcemia is a predictor of in-hospital mortality in patients with ischemic cerebrovascular disease.
Materials and methods
Case-control study. I included medical records of 162 patients 1:1 (81 cases and 81 controls), seen between 2015 and 2018. The odds ratio (OR) was calculated and a multivariate logistic regression analysis was performed to evaluate hypocalcemia as a predictor of mortality in ischemic stroke.
Results
Ionic calcium was significantly lower in the deceased than in the controls (0.73 and 0.41 mmol/L, respectively, p < 0.001), with hypocalcemia being an independent predictor of mortality after multivariate analysis (ORa: 2.58; 95%CI).: 1.16-9.01). Likewise, the intervening factors evaluated were arterial hypertension (ORa: 5.13, 95%CI: 2.41-10.94), diabetes mellitus (ORa: 2.58, 95%CI: 1.18-5.62), previous stroke (ORa: 1.85, 95%CI).: 1.62-5.52) and presenting high c-reactive protein (ORa: 2.23, 95% CI: 1.92-5.42), the predictive factors that remained significant after performing the multivariate adjustment.
Conclusion
It is concluded that hypocalcemia is a predictor of in-hospital mortality due to ischemic stroke.
{"title":"Hipocalcemia como factor asociado a mortalidad en enfermedad cerebrovascular isquémica","authors":"Angela Francesca Espinoza Baigorria , Elías Cabanillas Mejía , Carlos Zavaleta-Corvera , Maria Isabel De la Cruz Davila , Jose Caballero-Alvarado","doi":"10.1016/j.neuarg.2025.08.001","DOIUrl":"10.1016/j.neuarg.2025.08.001","url":null,"abstract":"<div><h3>Introduction</h3><div>There is evidence that calcium plays an important role in the pathogenesis of ischemic cerebrovascular accident (CVA), relating to the extent of ischemia and, therefore, to the patient's prognosis. This study aimed to determine if hypocalcemia is a predictor of in-hospital mortality in patients with ischemic cerebrovascular disease.</div></div><div><h3>Materials and methods</h3><div>Case-control study. I included medical records of 162 patients 1:1 (81 cases and 81 controls), seen between 2015 and 2018. The odds ratio (OR) was calculated and a multivariate logistic regression analysis was performed to evaluate hypocalcemia as a predictor of mortality in ischemic stroke.</div></div><div><h3>Results</h3><div>Ionic calcium was significantly lower in the deceased than in the controls (0.73 and 0.41 mmol/L, respectively, p<!--> <!--><<!--> <!-->0.001), with hypocalcemia being an independent predictor of mortality after multivariate analysis (ORa: 2.58; 95%CI).: 1.16-9.01). Likewise, the intervening factors evaluated were arterial hypertension (ORa: 5.13, 95%CI: 2.41-10.94), diabetes mellitus (ORa: 2.58, 95%CI: 1.18-5.62), previous stroke (ORa: 1.85, 95%CI).: 1.62-5.52) and presenting high c-reactive protein (ORa: 2.23, 95% CI: 1.92-5.42), the predictive factors that remained significant after performing the multivariate adjustment.</div></div><div><h3>Conclusion</h3><div>It is concluded that hypocalcemia is a predictor of in-hospital mortality due to ischemic stroke.</div></div>","PeriodicalId":39051,"journal":{"name":"Neurologia Argentina","volume":"17 4","pages":"Pages 234-241"},"PeriodicalIF":0.0,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145766078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-01DOI: 10.1016/j.neuarg.2025.06.004
Alberto Guevara Tirado
Introduction
Neurogranin is key in synaptic signaling. Understanding its interaction with beta-amyloid protein is crucial. Proteins such as SYT1, GAP43, and SNAP25 could mediate this effect.
Objective
To determine whether neurogranin is modulated by beta-amyloid protein through its interaction with synaptic biomarkers in preclinical stages of Alzheimer's disease.
Materials and methods
This is a secondary data analysis study consisting of 339 adults with and without the presence of beta-amyloid in cerebrospinal fluid (CSF) and/or positron emission tomography. CSF concentrations of neurogranin, SYT1, GAP43, and SNAP25 were analyzed. A parallel mediation model (Hayes PROCESS 4 model) was used to estimate the direct and indirect effects of amyloid-beta on neurogranin, mediated by synaptic biomarkers. The significance of indirect effects was assessed using bootstrapping with 5,000 resamples, generating 95% confidence intervals.
Results
Multiple linear regression models showed significant associations between amyloid-beta and SYT1, GAP43, and SNAP25. The coefficients were 34.104 (SYT1), 3.652464 (GAP43), and 12.371 (SNAP25); however, there was no significant direct effect between amyloid-beta and neurogranin (p = 0.688). The indirect effects through SYT1 and GAP43 showed significant influences on neurogranin (effects of 269,921 and 658,495, respectively). The indirect effect mediated by SNAP25 was not significant.
Conclusions
Although beta-amyloid protein was not directly associated with neurogranin, its influence is exerted indirectly through synaptic mediators such as SYT1 and GAP43. These findings reinforce the importance of synaptic pathways in preclinical stages of Alzheimer's disease.
{"title":"Interacciones entre beta-amiloide y proteínas sinápticas en la modulación de neurogranina en la fase preclínica de la enfermedad de Alzheimer","authors":"Alberto Guevara Tirado","doi":"10.1016/j.neuarg.2025.06.004","DOIUrl":"10.1016/j.neuarg.2025.06.004","url":null,"abstract":"<div><h3>Introduction</h3><div>Neurogranin is key in synaptic signaling. Understanding its interaction with beta-amyloid protein is crucial. Proteins such as SYT1, GAP43, and SNAP25 could mediate this effect.</div></div><div><h3>Objective</h3><div>To determine whether neurogranin is modulated by beta-amyloid protein through its interaction with synaptic biomarkers in preclinical stages of Alzheimer's disease.</div></div><div><h3>Materials and methods</h3><div>This is a secondary data analysis study consisting of 339 adults with and without the presence of beta-amyloid in cerebrospinal fluid (CSF) and/or positron emission tomography. CSF concentrations of neurogranin, SYT1, GAP43, and SNAP25 were analyzed. A parallel mediation model (Hayes PROCESS 4 model) was used to estimate the direct and indirect effects of amyloid-beta on neurogranin, mediated by synaptic biomarkers. The significance of indirect effects was assessed using bootstrapping with 5,000 resamples, generating 95% confidence intervals.</div></div><div><h3>Results</h3><div>Multiple linear regression models showed significant associations between amyloid-beta and SYT1, GAP43, and SNAP25. The coefficients were 34.104 (SYT1), 3.652464 (GAP43), and 12.371 (SNAP25); however, there was no significant direct effect between amyloid-beta and neurogranin (p<!--> <!-->=<!--> <!-->0.688). The indirect effects through SYT1 and GAP43 showed significant influences on neurogranin (effects of 269,921 and 658,495, respectively). The indirect effect mediated by SNAP25 was not significant.</div></div><div><h3>Conclusions</h3><div>Although beta-amyloid protein was not directly associated with neurogranin, its influence is exerted indirectly through synaptic mediators such as SYT1 and GAP43. These findings reinforce the importance of synaptic pathways in preclinical stages of Alzheimer's disease.</div></div>","PeriodicalId":39051,"journal":{"name":"Neurologia Argentina","volume":"17 4","pages":"Pages 227-233"},"PeriodicalIF":0.0,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145766077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-01DOI: 10.1016/j.neuarg.2025.05.006
Tomás Martín Cosacov , Susana Liwacki
Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system and the leading cause of non-traumatic neurological disability in young adults. An early diagnosis is crucial for initiating disease-modifying treatments and preventing the progression of disability. However, multiple factors can delay diagnosis and treatment initiation. The objective of this study was to identify these factors and their impact on time to diagnosis and treatment in a cohort of patients at Hospital Córdoba. The researchers conducted a cross-sectional observational study of 153 adult patients diagnosed with multiple sclerosis according to the 2017 McDonald criteria. Their clinical and demographic data were collected and analyzed using logistic regression to determine the factors associated with an early versus late diagnosis or early versus late treatment initiation. The median times to diagnosis and treatment initiation were 95 and 184 days, respectively. Factors such as clinical onset with optic neuritis, diplopia, or motor symptoms were associated with an early diagnosis. In contrast, lack of health insurance, delays in test authorization, and delays in medication dispensing were relevant factors in late treatment initiation, though not statistically significant. Delaying consultation with a specialist was a significant predictor of late treatment initiation. This study highlights the frequency of late diagnosis of multiple sclerosis at Hospital Córdoba, which impacts the progression of disability. Specific clinical factors can favor early diagnosis, while barriers to access and delays in care can complicate the timely initiation of treatment. Improving health education and access to diagnostic resources for vulnerable populations could reduce these delays and improve patient outcomes.
{"title":"Retraso diagnóstico de esclerosis múltiple y sus factores asociados en los pacientes del Hospital Córdoba. Desafíos en la identificación precoz de la enfermedad en un centro de referencia","authors":"Tomás Martín Cosacov , Susana Liwacki","doi":"10.1016/j.neuarg.2025.05.006","DOIUrl":"10.1016/j.neuarg.2025.05.006","url":null,"abstract":"<div><div>Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system and the leading cause of non-traumatic neurological disability in young adults. An early diagnosis is crucial for initiating disease-modifying treatments and preventing the progression of disability. However, multiple factors can delay diagnosis and treatment initiation. The objective of this study was to identify these factors and their impact on time to diagnosis and treatment in a cohort of patients at Hospital Córdoba. The researchers conducted a cross-sectional observational study of 153 adult patients diagnosed with multiple sclerosis according to the 2017 McDonald criteria. Their clinical and demographic data were collected and analyzed using logistic regression to determine the factors associated with an early versus late diagnosis or early versus late treatment initiation. The median times to diagnosis and treatment initiation were 95 and 184 days, respectively. Factors such as clinical onset with optic neuritis, diplopia, or motor symptoms were associated with an early diagnosis. In contrast, lack of health insurance, delays in test authorization, and delays in medication dispensing were relevant factors in late treatment initiation, though not statistically significant. Delaying consultation with a specialist was a significant predictor of late treatment initiation. This study highlights the frequency of late diagnosis of multiple sclerosis at Hospital Córdoba, which impacts the progression of disability. Specific clinical factors can favor early diagnosis, while barriers to access and delays in care can complicate the timely initiation of treatment. Improving health education and access to diagnostic resources for vulnerable populations could reduce these delays and improve patient outcomes.</div></div>","PeriodicalId":39051,"journal":{"name":"Neurologia Argentina","volume":"17 3","pages":"Pages 181-189"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145021075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-01DOI: 10.1016/j.neuarg.2025.05.002
Edgar Castillo-Tamara , Loida Camargo , María Cecilia Díaz , Nicole Caldichoury , Jorge Herrera-Pino , Juan-Carlos Coronado , Yuliana Florez , Daniela Ripoll-Córdoba , Juan Camilo Benitez-Agudelo , Norman López
Introduction
Currently, there is evidence of numerous neurological manifestations in patients with various complications associated with COVID-19, one of which is stroke.
Clinical case
We present a young patient with no prior comorbidities and asymptomatic COVID-19, who developed motor aphasia as a manifestation of ischemic stroke.
Conclusion
We aim to highlight the importance of testing for SARS-CoV-2 in patients with cerebral ischemia without any other probable cause, even if they do not present symptoms of COVID-19.
{"title":"Ictus isquémico en una paciente de 27 años con COVID-19 asintomático: informe de un caso","authors":"Edgar Castillo-Tamara , Loida Camargo , María Cecilia Díaz , Nicole Caldichoury , Jorge Herrera-Pino , Juan-Carlos Coronado , Yuliana Florez , Daniela Ripoll-Córdoba , Juan Camilo Benitez-Agudelo , Norman López","doi":"10.1016/j.neuarg.2025.05.002","DOIUrl":"10.1016/j.neuarg.2025.05.002","url":null,"abstract":"<div><h3>Introduction</h3><div>Currently, there is evidence of numerous neurological manifestations in patients with various complications associated with COVID-19, one of which is stroke.</div></div><div><h3>Clinical case</h3><div>We present a young patient with no prior comorbidities and asymptomatic COVID-19, who developed motor aphasia as a manifestation of ischemic stroke.</div></div><div><h3>Conclusion</h3><div>We aim to highlight the importance of testing for SARS-CoV-2 in patients with cerebral ischemia without any other probable cause, even if they do not present symptoms of COVID-19.</div></div>","PeriodicalId":39051,"journal":{"name":"Neurologia Argentina","volume":"17 3","pages":"Pages 197-202"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145021077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-01DOI: 10.1016/j.neuarg.2025.06.003
Andrés Barboza , María Cecilia Fernández , Javier Hryb , Manuel Facundo Latini , Carlos Alberto Mangone , Analisa Manin , Mariano Marrodan , Nahuel Pereira de Silva , Manuel Pérez Akly , Galeno Rojas , Lucas Romano , Carlos Rugilo , Marina Sánchez , Martin Tourreilles , Andrés Villa , Florencia Yorio , Daniel Zuin
Introduction
Autoimmune encephalitis (AE) is a rapidly evolving field in neurology, with improved recognition due to advances in antibody detection. Despite its growing incidence, diagnostic and therapeutic challenges persist, including clinical heterogeneity, risk of misdiagnosis, and lack of standardized protocols. The Argentine Consensus on Diagnosis and Treatment of Autoimmune Encephalitis in Adults (CARENAI), endorsed by the Argentine Neurological Society, aims to establish management guidelines for AE in Argentina.
Methods
Seventeen experts from various neurological subspecialties were convened, using the RAND/UCLA method to evaluate diagnostic and therapeutic strategies. A systematic literature review informed the recommendations, focusing on clinical suspicion, antibody testing (in CSF and serum), neuroimaging (MRI, PET-FDG), EEG interpretation, and immunotherapeutic approaches.
Results
Diagnostic criteria emphasize subacute cognitive/psychiatric symptoms, exclusion of differential diagnoses, and inflammatory findings in CSF/MRI. First-line treatment includes corticosteroids, intravenous immunoglobulins (IVIG), or plasmapheresis, while refractory cases may require rituximab or cyclophosphamide. CARENAI addresses phenotype-specific management and emphasizes early tumor screening in paraneoplastic cases. Prognostic factors and relapse prevention are discussed, highlighting the importance of interdisciplinary follow-up.
Conclusion
CARENAI provides a framework to reduce diagnostic delays, optimize treatments, and improve outcomes, while acknowledging evidence gaps. It advocates for improved access to specialized testing and promotes future research to refine AE management in Argentina.
{"title":"Consenso Argentino de Diagnóstico y Tratamiento de Encefalitis Autoinmune en Adultos (CARENAI)","authors":"Andrés Barboza , María Cecilia Fernández , Javier Hryb , Manuel Facundo Latini , Carlos Alberto Mangone , Analisa Manin , Mariano Marrodan , Nahuel Pereira de Silva , Manuel Pérez Akly , Galeno Rojas , Lucas Romano , Carlos Rugilo , Marina Sánchez , Martin Tourreilles , Andrés Villa , Florencia Yorio , Daniel Zuin","doi":"10.1016/j.neuarg.2025.06.003","DOIUrl":"10.1016/j.neuarg.2025.06.003","url":null,"abstract":"<div><h3>Introduction</h3><div>Autoimmune encephalitis (AE) is a rapidly evolving field in neurology, with improved recognition due to advances in antibody detection. Despite its growing incidence, diagnostic and therapeutic challenges persist, including clinical heterogeneity, risk of misdiagnosis, and lack of standardized protocols. The Argentine Consensus on Diagnosis and Treatment of Autoimmune Encephalitis in Adults (CARENAI), endorsed by the Argentine Neurological Society, aims to establish management guidelines for AE in Argentina.</div></div><div><h3>Methods</h3><div>Seventeen experts from various neurological subspecialties were convened, using the RAND/UCLA method to evaluate diagnostic and therapeutic strategies. A systematic literature review informed the recommendations, focusing on clinical suspicion, antibody testing (in CSF and serum), neuroimaging (MRI, PET-FDG), EEG interpretation, and immunotherapeutic approaches.</div></div><div><h3>Results</h3><div>Diagnostic criteria emphasize subacute cognitive/psychiatric symptoms, exclusion of differential diagnoses, and inflammatory findings in CSF/MRI. First-line treatment includes corticosteroids, intravenous immunoglobulins (IVIG), or plasmapheresis, while refractory cases may require rituximab or cyclophosphamide. CARENAI addresses phenotype-specific management and emphasizes early tumor screening in paraneoplastic cases. Prognostic factors and relapse prevention are discussed, highlighting the importance of interdisciplinary follow-up.</div></div><div><h3>Conclusion</h3><div>CARENAI provides a framework to reduce diagnostic delays, optimize treatments, and improve outcomes, while acknowledging evidence gaps. It advocates for improved access to specialized testing and promotes future research to refine AE management in Argentina.</div></div>","PeriodicalId":39051,"journal":{"name":"Neurologia Argentina","volume":"17 3","pages":"Pages 153-172"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145019290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-01DOI: 10.1016/j.neuarg.2025.06.005
Alberto Guevara Tirado
Introduction
Cardiometabolic alterations affect glycemic control, but the modulatory role of cerebral white matter lesions in these associations is not yet fully understood.
Objective
To evaluate whether the presence of cerebral white matter lesions moderates the relationship between BMI and glucose through cardiometabolic markers.
Materials and Methods
Analytical secondary data study (n = 1904) of patients undergoing clinical evaluations and brain MRI. The independent variable was BMI and fasting glucose the dependent variable; mediators included LDL, triglycerides (TG), and systolic blood pressure (SBP); and the moderator was the presence of cerebral white matter lesions. Hayes’ PROCESS model 59 was used to assess direct, indirect, and moderated effects. The causal model was visualized with a directed acyclic graph.
Results
The effect of BMI on LDL (β = 1.47; p < 0.001), TG (β = 10.13; p < 0.001), and SBP(β = 1.45; p < 0.001) was attenuated in the presence of lesions, with significant negative interactions (LDL: β = −0.86; p = 0.036; TG: β = −3.89; p = 0.003; SBP: β = −0.81; p = 0.001). In the glucose model, BMI (β = 1.36; p < 0.001), TG (β = 0.015; p = 0.003), and SBP (β = 0.11; p = 0.004) showed positive associations. Lesions had no significant direct effect (β = 11.58; p = 0.12) but moderated the BMI-glucose (interaction: β = −0.49; p = 0.048) and TG-glucose (interaction: β = 0.058; p < 0.001) relationships. The indirect effect of BMI on glucose via triglycerides was greater in the presence of lesions (β = 0.45; 95%CI: 0.25–0.75) than in their absence (β = 0.15;95%CI: 0.01-0.40). Mediation through SBP was significant in both groups (no lesions: β = 0.15; with lesions: β = 0.07).
Conclusions
The indirect effects of BMI on glucose are modulated by the presence of cerebral white matter lesions, highlighting the modulatory role of brain damage in the pathways linking adiposity and glycemic control.
心脏代谢改变影响血糖控制，但脑白质病变在这些关联中的调节作用尚不完全清楚。目的探讨脑白质病变是否通过心脏代谢指标调节BMI与血糖的关系。材料与方法分析性二次资料研究（n = 1904）进行临床评估和脑MRI检查的患者。自变量为BMI，因变量为空腹血糖；介质包括LDL、甘油三酯（TG）和收缩压（SBP）；大脑白质损伤的出现是缓和因素。Hayes的PROCESS模型59用于评估直接、间接和调节效应。用有向无环图将因果模型可视化。结果BMI对LDL （β = 1.47; p < 0.001）、TG （β = 10.13; p < 0.001）和收缩压（β = 1.45; p < 0.001）的影响在病变存在时减弱，存在显著的负相互作用（LDL: β = - 0.86; p = 0.036; TG: β = - 3.89; p = 0.003；收缩压：β = - 0.81; p = 0.001）。在葡萄糖模型中，BMI （β = 1.36; p < 0.001）、TG （β = 0.015; p = 0.003）和收缩压（β = 0.11; p = 0.004）呈正相关。病变对bmi -葡萄糖（相互作用：β = - 0.49; p = 0.048）和tg -葡萄糖（相互作用：β = 0.058; p < 0.001）关系没有显著的直接影响（β = 11.58; p = 0.12）。存在病变时，BMI通过甘油三酯对葡萄糖的间接影响（β = 0.45; 95%CI: 0.25-0.75）大于无病变时（β = 0.15;95%CI: 0.01-0.40）。两组通过收缩压介导均显著（无病变：β = 0.15；有病变：β = 0.07）。结论BMI对血糖的间接影响受到脑白质损伤的调节，突出了脑损伤在肥胖和血糖控制通路中的调节作用。
{"title":"El rol modulador de lesiones en sustancia blanca en la mediación entre IMC, lípidos, presión arterial y niveles de glucosa","authors":"Alberto Guevara Tirado","doi":"10.1016/j.neuarg.2025.06.005","DOIUrl":"10.1016/j.neuarg.2025.06.005","url":null,"abstract":"<div><h3>Introduction</h3><div>Cardiometabolic alterations affect glycemic control, but the modulatory role of cerebral white matter lesions in these associations is not yet fully understood.</div></div><div><h3>Objective</h3><div>To evaluate whether the presence of cerebral white matter lesions moderates the relationship between BMI and glucose through cardiometabolic markers.</div></div><div><h3>Materials and Methods</h3><div>Analytical secondary data study (n<!--> <!-->=<!--> <!-->1904) of patients undergoing clinical evaluations and brain MRI. The independent variable was BMI and fasting glucose the dependent variable; mediators included LDL, triglycerides (TG), and systolic blood pressure (SBP); and the moderator was the presence of cerebral white matter lesions. Hayes’ PROCESS model 59 was used to assess direct, indirect, and moderated effects. The causal model was visualized with a directed acyclic graph.</div></div><div><h3>Results</h3><div>The effect of BMI on LDL (β<!--> <!-->=<!--> <!-->1.47; p<!--> <!--><<!--> <!-->0.001), TG (β<!--> <!-->=<!--> <!-->10.13; p<!--> <!--><<!--> <!-->0.001), and SBP(β<!--> <!-->=<!--> <!-->1.45; p<!--> <!--><<!--> <!-->0.001) was attenuated in the presence of lesions, with significant negative interactions (LDL: β<!--> <!-->=<!--> <!-->−0.86; p<!--> <!-->=<!--> <!-->0.036; TG: β<!--> <!-->=<!--> <!-->−3.89; p<!--> <!-->=<!--> <!-->0.003; SBP: β<!--> <!-->=<!--> <!-->−0.81; p<!--> <!-->=<!--> <!-->0.001). In the glucose model, BMI (β<!--> <!-->=<!--> <!-->1.36; p<!--> <!--><<!--> <!-->0.001), TG (β<!--> <!-->=<!--> <!-->0.015; p<!--> <!-->=<!--> <!-->0.003), and SBP (β<!--> <!-->=<!--> <!-->0.11; p<!--> <!-->=<!--> <!-->0.004) showed positive associations. Lesions had no significant direct effect (β<!--> <!-->=<!--> <!-->11.58; p<!--> <!-->=<!--> <!-->0.12) but moderated the BMI-glucose (interaction: β<!--> <!-->=<!--> <!-->−0.49; p<!--> <!-->=<!--> <!-->0.048) and TG-glucose (interaction: β<!--> <!-->=<!--> <!-->0.058; p<!--> <!--><<!--> <!-->0.001) relationships. The indirect effect of BMI on glucose via triglycerides was greater in the presence of lesions (β<!--> <!-->=<!--> <!-->0.45; 95%<span>C</span>I: 0.25–0.75) than in their absence (β<!--> <!-->=<!--> <!-->0.15;95%CI: 0.01-0.40). Mediation through SBP was significant in both groups (no lesions: β<!--> <!-->=<!--> <!-->0.15; with lesions: β<!--> <!-->=<!--> <!-->0.07).</div></div><div><h3>Conclusions</h3><div>The indirect effects of BMI on glucose are modulated by the presence of cerebral white matter lesions, highlighting the modulatory role of brain damage in the pathways linking adiposity and glycemic control.</div></div>","PeriodicalId":39051,"journal":{"name":"Neurologia Argentina","volume":"17 3","pages":"Pages 173-180"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145019291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-01DOI: 10.1016/j.neuarg.2025.05.001
Otto J. Hernández Fustes , Carlos Arteaga Rodríguez
{"title":"Trombosis venosa cerebral: experiencia en un hospital de referencia nacional del Perú","authors":"Otto J. Hernández Fustes , Carlos Arteaga Rodríguez","doi":"10.1016/j.neuarg.2025.05.001","DOIUrl":"10.1016/j.neuarg.2025.05.001","url":null,"abstract":"","PeriodicalId":39051,"journal":{"name":"Neurologia Argentina","volume":"17 3","pages":"Pages 211-212"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145019287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Neurological disorders present a significant global health challenge, with limited effective treatment options due to the complex and selective nature of the blood–brain barrier (BBB). Recent years have witnessed remarkable advancements in nanoparticle-based drug delivery systems designed to overcome these barriers and enhance the therapeutic outcomes of neurological disorder treatments. Among these innovations, nasal drug delivery has emerged as a promising non-invasive approach to bypass the BBB and directly target the central nervous system (CNS). This article provides an overview of the origin of nanotechnology and its intersection with biotechnology, leading to the emergence of nanobiotechnology. It highlights the role of nanotechnology in drug delivery and its potential to enhance the effectiveness of nanoscale structures in biomedical science. The article emphasizes the significance of the chemical composition of nanoparticles (NPs) in determining their physiochemical properties and drug-release behavior. The challenges posed by the BBB in delivering drugs to the CNS and the limited permeability of macromolecules to the barrier. The article emphasizes the role of the BBB as a diffusion barrier and explains the mechanisms by which molecules can cross the barrier. It mentions the presence of interendothelial junctions and receptors/transporters in endothelial cells that regulate the permeability of the BBB. Overall, the article provides an overview of the role of nanoparticles in drug delivery through the nasal route for the treatment of neurological disorders.
{"title":"Recent advancements in nanoparticle drug delivery systems to cure neurological disorders via the nasal route","authors":"Preeti Tiwari , S.K. Prajapati , Vihangesh Dixit , Mohammad Adnan Raza , Ajazuddin , Sanjay Kumar Gupta , Mukesh Sharma","doi":"10.1016/j.neuarg.2025.05.003","DOIUrl":"10.1016/j.neuarg.2025.05.003","url":null,"abstract":"<div><div>Neurological disorders present a significant global health challenge, with limited effective treatment options due to the complex and selective nature of the blood–brain barrier (BBB). Recent years have witnessed remarkable advancements in nanoparticle-based drug delivery systems designed to overcome these barriers and enhance the therapeutic outcomes of neurological disorder treatments. Among these innovations, nasal drug delivery has emerged as a promising non-invasive approach to bypass the BBB and directly target the central nervous system (CNS). This article provides an overview of the origin of nanotechnology and its intersection with biotechnology, leading to the emergence of nanobiotechnology. It highlights the role of nanotechnology in drug delivery and its potential to enhance the effectiveness of nanoscale structures in biomedical science. The article emphasizes the significance of the chemical composition of nanoparticles (NPs) in determining their physiochemical properties and drug-release behavior. The challenges posed by the BBB in delivering drugs to the CNS and the limited permeability of macromolecules to the barrier. The article emphasizes the role of the BBB as a diffusion barrier and explains the mechanisms by which molecules can cross the barrier. It mentions the presence of interendothelial junctions and receptors/transporters in endothelial cells that regulate the permeability of the BBB. Overall, the article provides an overview of the role of nanoparticles in drug delivery through the nasal route for the treatment of neurological disorders.</div></div>","PeriodicalId":39051,"journal":{"name":"Neurologia Argentina","volume":"17 3","pages":"Pages 143-152"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145019289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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