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Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses
Published on: June 14, 2020
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Ciencia básica y patogénesis
Fernanda G Q Barros-Aragão1, Luis E Santos1, Talita Pinto2
1D'Or Institute for Research and Education, Rio de Janeiro, RJ, Brazil.
Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 25, 2025
Resumen
Los pacientes neurológicos con COVID-19 muestran una proteína Tau elevada, similar a los pacientes con enfermedad de Alzheimer (EA), relacionada con la inflamación. La inflamación persistente y los problemas cognitivos posteriores al COVID-19 pueden aumentar el riesgo futuro de EA.
Área de la Ciencia:
- Neurociencia; Inmunología; Enfermedades Infecciosas
Sus antecedentes:
- El COVID-19 puede causar síntomas neurológicos y deterioro cognitivo, y la enfermedad de Alzheimer (EA) aumenta la gravedad del COVID-19.; La inflamación está implicada tanto en el COVID-19 como en la EA, lo que sugiere un posible vínculo molecular.; Aún no está claro si los pacientes con COVID-19 con problemas neurológicos presentan cambios moleculares relacionados con la EA.
Objetivo del estudio:
- Investigar las alteraciones moleculares relacionadas con la patología de la enfermedad de Alzheimer (EA) en pacientes con COVID-19 con síntomas neurológicos.; Identificar posibles vínculos moleculares entre COVID-19 y EA para mejorar el seguimiento de los pacientes y las estrategias de prevención.
Principales métodos:
- Análisis retrospectivo de biomarcadores en líquido cefalorraquídeo (LCR) (amiloide-beta, Tau) en controles, deterioro cognitivo leve, EA y pacientes con COVID-19 con síntomas neurológicos.; Correlación de biomarcadores del LCR con marcadores de inflamación (IL6, SII).; Evaluación prospectiva de biomarcadores en plasma (amiloide-beta, Tau) y resultados cognitivos en supervivientes de COVID-19 hasta un año después de la infección.
Principales resultados:
- Los pacientes con COVID-19 con síntomas neurológicos mostraron niveles elevados de Tau en el LCR en el momento de la hospitalización, similar a los pacientes con EA.; No se detectaron cambios significativos en los niveles de amiloide-beta o pTau-181 en el LCR en pacientes con COVID-19.; Los biomarcadores del LCR y las citoquinas proinflamatorias se correlacionaron con la inflamación sistémica (SII).; La relación Tau/amiloide-beta en plasma aumentó en los supervivientes de COVID-19 con déficits cognitivos un año después de la infección.; Los cambios longitudinales de Tau en plasma se vieron influenciados por la gravedad de la enfermedad, la inflamación y los déficits cognitivos.
Conclusiones:
- La inflamación es un factor clave en los cambios moleculares agudos y persistentes relacionados con la EA observados en pacientes con COVID-19.; Los supervivientes de COVID-19 con inflamación continua o síntomas cognitivos requieren una monitorización cuidadosa del posible riesgo futuro de EA.
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