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Summary
This summary is machine-generated.

Higher phasic activity in the locus coeruleus (LC) may protect against Alzheimer's disease (AD) tau pathology and cognitive decline. This study linked lower LC activity to increased tau deposition and faster memory decline in older adults.

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Area of Science:

  • Neuroscience
  • Neuroimaging
  • Alzheimer's Disease Research

Background:

  • The locus coeruleus (LC), a brainstem nucleus, is an early site of Alzheimer's disease (AD) tau accumulation.
  • Reduced novelty-related LC activity in healthy older adults correlates with increased entorhinal cortex (EC) tau and memory decline.
  • Animal models suggest LC activation can confer resilience against tau's cognitive effects.

Purpose of the Study:

  • To investigate the association between in-vivo phasic-like LC activity and cortical tau deposition in asymptomatic older adults.
  • To examine the relationship between LC activity, EC tau accumulation, and longitudinal cognitive decline.

Main Methods:

  • Ninety-two cognitively healthy older adults underwent baseline tau-PET and resting-state fMRI.
  • Phasic-like LC activity was identified using a novel minimum entropy-based algorithm applied to BOLD data.
  • Associations between LC activity, tau deposition (FTP-PET), and cognitive decline (PACC5) were analyzed using regression and mixed-effects models.

Main Results:

  • Lower phasic LC activity was significantly associated with greater baseline EC tau deposition and faster medial temporal lobe tau accumulation.
  • Reduced phasic LC activity correlated with steeper cognitive decline, particularly in memory-related functions.
  • The negative impact of LC activity on cognitive decline was exacerbated by higher levels of inferior-temporal tau.

Conclusions:

  • Elevated phasic LC activity appears to be neuroprotective, potentially delaying tau accumulation in early AD-related regions and mitigating adverse cognitive effects.
  • These findings support the role of LC phasic activity in AD pathogenesis and suggest it as a potential therapeutic target for early intervention.
  • Targeting LC phasic activity could offer a novel strategy to delay cognitive decline in aging and preclinical AD.