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A Metadata Extraction Approach for Clinical Case Reports to Enable Advanced Understanding of Biomedical Concepts
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Manifestaciones Clínicas

Deepti Putcha1, Kanella Basilion2, Yuta Katsumi1

  • 1Frontotemporal Disorders Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.

Alzheimer's & dementia : the journal of the Alzheimer's Association
|December 24, 2025
PubMed
Resumen
Este resumen es generado por máquina.

Las variantes atípicas de la enfermedad de Alzheimer (EA) muestran déficits en la codificación y el almacenamiento de la memoria. La EA de inicio temprano (EOAD) tiene una pérdida de memoria más rápida, mientras que la atrofia cortical posterior (PCA) y la afasia primaria progresiva logopénica (lvPPA) difieren en la vinculación de la memoria espacial.

Palabras clave:
Enfermedad de Alzheimer atípicaDéficits de memoriaEOADPCAlvPPANeuropsicología

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Área de la Ciencia:

  • Neurociencia
  • Neurología
  • Ciencia Cognitiva

Sus antecedentes:

  • Los criterios de diagnóstico de la enfermedad de Alzheimer (EA) sugieren memoria episódica preservada en las primeras etapas, pero ocurren déficits de memoria en variantes atípicas como la atrofia cortical posterior (PCA) y la afasia primaria progresiva logopénica (lvPPA).
  • Los distintos patrones de deterioro de la memoria en síndromes de EA no amnésicos siguen sin estar claros.
  • Este estudio investiga los déficits de memoria en la EA de inicio temprano (EOAD), lvPPA y PCA.

Objetivo del estudio:

  • Caracterizar y comparar los déficits de memoria en síndromes atípicos de la enfermedad de Alzheimer (EA).
  • Investigar los patrones compartidos y disociables de deterioro de la memoria.
  • Explorar la relación entre la atrofia cerebral y el rendimiento de la memoria.

Principales métodos:

  • Se evaluó a 16 participantes con EA de inicio temprano (EOAD), 9 con lvPPA, 21 con PCA y 29 controles cognitivamente sanos (CN).
  • Se utilizó una nueva prueba de memoria de objetos y ubicaciones (OLMT) para evaluar la memoria asociativa sin demandas léxicas.
  • Se utilizaron análisis de varianza (ANOVA) y modelos lineales generales para analizar el rendimiento del grupo y las correlaciones de atrofia cerebral.

Principales resultados:

  • Todas las variantes atípicas de EA mostraron una codificación y almacenamiento deteriorados en comparación con los controles.
  • La EOAD mostró una mayor pérdida de almacenamiento en el recuerdo a los 3 minutos que la PCA y la lvPPA.
  • La lvPPA se destacó en la asociación y retención de la ubicación de objetos, a diferencia de la EOAD y la PCA, que tuvieron dificultades en la codificación y retención de ubicaciones espaciales.

Conclusiones:

  • Los síndromes atípicos de EA presentan déficits de codificación y almacenamiento, ampliando la caracterización de la EA no amnésica.
  • La EOAD muestra una pérdida acelerada de almacenamiento, lo que sugiere un posible deterioro multidominio.
  • Los déficits distintos en la vinculación de la memoria espacial diferencian la PCA y la lvPPA, lo que ayuda en el diagnóstico y el entrenamiento cognitivo específico.