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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.
Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 23, 2025
Summary
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.
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.
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