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Tengfei Li1, Xifeng Wang1, Martin Cole2

  • 1University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.

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|December 24, 2025
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Resumen
Este resumen es generado por máquina.

El amiloide-beta (Aβ) impacta el deterioro cognitivo en la enfermedad de Alzheimer (EA) en parte a través de cambios en la conectividad estructural del cerebro, específicamente la anisotropía fraccional (FA) en las redes visual, del modo por defecto (DMN) y frontoparietal (FPN).

Palabras clave:
Enfermedad de AlzheimerAmiloide-betaConectividad cerebralDeterioro cognitivoNeuroimagenAnisotropía fraccionalRedes cerebralesRed del modo por defectoRed frontoparietal

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Área de la Ciencia:

  • Neuroimaging
  • Neuroscience
  • Alzheimer's Disease Research

Sus antecedentes:

  • Alzheimer's Disease (AD) is characterized by cognitive decline.
  • Amyloid-beta (Aβ) accumulation is a key pathological hallmark of AD.
  • Brain structural connectivity alterations may mediate Aβ's effects on cognition.

Objetivo del estudio:

  • To investigate how brain structural connectivity mediates the impact of Aβ on cognitive decline in AD.
  • To identify specific brain networks and pathways involved in this mediation process.

Principales métodos:

  • Utilized fibertracking tractography and fiber clustering on the ADNI2 dataset.
  • Computed mean fractional anisotropy (FA) and analyzed associations with CSF Aβ42 and cognitive scores (MMSE).
  • Employed linear mixed models and FDR-adjusted mediation analyses, controlling for confounders.

Principales resultados:

  • 16 fibers showed mediation of Aβ's effect on MMSE, primarily within visual, DMN, and FPN networks.
  • Aβ positively associated with FA in DMN or FPN-related fibers during early AD phases.
  • FA changes mediated 21.6% of Aβ's impact on cognitive decline.

Conclusiones:

  • Brain structural connectivity, particularly FA within visual, DMN, and FPN networks, partially mediates Aβ's effect on cognitive decline in AD.
  • DMN and FPN connectivity are notably susceptible in the early stages of AD.