Elevated Norepinephrine Metabolism Gauges Alzheimer's Disease-Related Pathology and Memory Decline

J.M. Riphagen, M. van Egroo, H.I.L. Jacobs*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

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 languageEnglish
Pages (from-to)521-526
Number of pages6
JournalJournal of Alzheimer's Disease
Volume80
Issue number2
DOIs
Publication statusPublished - 2021

Keywords

  • Amyloid-beta
  • locus coeruleus
  • memory
  • norepinephrine
  • tau
  • DEMENTIA
  • TAU
  • NATIONAL INSTITUTE
  • PLASMA
  • RECOMMENDATIONS
  • MHPG
  • LOCUS-COERULEUS
  • DIAGNOSTIC GUIDELINES
  • ASSOCIATION WORKGROUPS

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