Abstract
The noradrenergic (NE) locus coeruleus (LC) is vulnerable to hyperphosphorylated tau, and dysregulated NE-metabolism is linked to greater tau and disease progression. We investigated whether elevated NE-metabolism alone predicts memory decline or whether concomitant presence of tau and amyloid-beta is required. Among 114 memory clinic participants, time trends (max. six years) showed dose-response declines in learning across groups with elevated NE-metabolite 3-methoxy4-hydroxyphenylethyleneglycol (MHPG) with no, one, or two Alzheimer's disease biomarkers; and no decline in the low MHPG group. Elevated MHPG is required and sufficient to detect learning declines, supporting a pathophysiologic model including the LC-NE system contributing to initial Alzheimer's disease-related processes.
Original language | English |
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Pages (from-to) | 521-526 |
Number of pages | 6 |
Journal | Journal of Alzheimer's Disease |
Volume | 80 |
Issue number | 2 |
DOIs | |
Publication status | Published - 2021 |
Keywords
- Amyloid-beta
- locus coeruleus
- memory
- norepinephrine
- tau
- DEMENTIA
- TAU
- NATIONAL INSTITUTE
- PLASMA
- RECOMMENDATIONS
- MHPG
- LOCUS-COERULEUS
- DIAGNOSTIC GUIDELINES
- ASSOCIATION WORKGROUPS