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Frontotemporal network connectivity during memory encoding is increased with aging and disrupted by beta-amyloid.

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Brain amyloid (Aβ) impacts memory in older adults. In those without Aβ, brain networks compensate for aging, but this compensation fails when Aβ is present, leading to memory decline.

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Area of Science:

  • Neuroscience
  • Cognitive Aging
  • Alzheimer's Disease Research

Background:

  • Alzheimer's disease (AD) is characterized by brain β-amyloid (Aβ) plaques.
  • Aβ deposition is found in 30% of cognitively normal older adults.
  • Aβ is linked to neural alterations and episodic memory decline.

Purpose of the Study:

  • To investigate how aging and Aβ deposition influence neural function during memory encoding.
  • To examine the role of functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) in assessing these effects.

Main Methods:

  • fMRI scans were performed on 36 cognitively normal older adults and 15 young adults.
  • PET scans with [(11)C] Pittsburgh compound B measured fibrillar brain Aβ in older adults.
  • Neural activation and functional connectivity during visual scene memory encoding were analyzed.

Main Results:

  • Older adults without Aβ showed reduced regional activation and decreased task-independent connectivity compared to young adults.
  • In older adults without Aβ, increased task-related connectivity correlated with memory performance.
  • Older adults with Aβ exhibited increased regional activity unrelated to performance and lacked compensatory network connectivity.

Conclusions:

  • Network connectivity compensates for reduced regional activity in successful memory encoding in aging without Aβ.
  • In the presence of Aβ, this compensatory network mechanism fails.
  • Aβ deposition is associated with inefficient regional hyperactivation during memory encoding.