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Basic Science and Pathogenesis.

Alfie Wearn1, Christine L Tardif2,3, Ilana R Leppert3,4

  • 1Montreal Neurological Institute, McGill University, Montreal, QC, Canada.

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|December 23, 2025
PubMed
Summary
This summary is machine-generated.

Locus coeruleus (LC) integrity is linked to amyloid and tau pathology in asymptomatic Alzheimer's disease (AD) individuals. This suggests the LC plays a key role in early AD pathogenesis, even before symptoms appear.

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Area of Science:

  • Neuroscience
  • Neuropathology
  • Radiology

Background:

  • The locus coeruleus (LC) is an early site of tau pathology in Alzheimer's disease (AD), preceding clinical symptoms.
  • Investigating LC integrity in relation to amyloid and tau deposition is crucial for understanding preclinical AD.

Purpose of the Study:

  • To determine if locus coeruleus (LC) integrity is associated with in vivo cortical amyloid and tau deposition in asymptomatic, at-risk older adults.
  • To explore the relationship between LC integrity and early AD hallmarks.

Main Methods:

  • Utilized 3T MRI and PET imaging (18F-NAV4694 for amyloid, 18F-flortaucipir for tau) in 208 healthy older adults with a family history of AD.
  • Quantified LC integrity using neuromelanin-sensitive brainstem imaging (LCCNR) and regional cortical amyloid/tau deposition (SUVR).
  • Employed robust linear mixed-effects models and linear regression, correcting for age, sex, and education, with FDR adjustment for p-values.

Main Results:

  • Negative associations were found between LC integrity and cortical amyloid SUVR across most regions.
  • LC integrity showed associations with cortical tau in temporal and inferior parietal regions, particularly in the left hemisphere.
  • These associations were present at baseline, not longitudinally, and the tau-LC relationship was modulated by global amyloid levels.

Conclusions:

  • Locus coeruleus (LC) degeneration correlates with increased amyloid and tau pathology in asymptomatic individuals with AD risk factors.
  • These findings support the model of the LC as a central player in the earliest pathophysiological changes of Alzheimer's disease.