Human brain myelination and amyloid beta deposition in Alzheimer's disease

George Bartzokis, Po H. Lu, Jim Mintz

Research output: Contribution to journalArticle

90 Scopus citations

Abstract

We hypothesized that myelin breakdown in vulnerable late-myelinating regions releases oligodendrocyte- and myelin-associated iron that promotes amyloid beta (Aβ) oligomerization, its associated toxicity, and the deposition of oligomerized Aβ and iron in neuritic plaques observed in Alzheimer's disease (AD). The model was tested by using published maps of cortical myelination from 1901 and recent in vivo imaging maps of Aβ deposits in humans. The data show that in AD, radiolabeled ligands detect Aβ deposition in a distribution that matches the map of late-myelinating regions. Furthermore, the strikingly lower ability of this imaging ligand to bind Aβ in animal models is consistent with the much lower levels of myelin and associated iron levels in rodents when compared with humans. The hypotheses derived from the "myelin model" are testable with current imaging methods and have important implications for therapeutic interventions that should be expanded to include novel targets such as oligodendrocytes, myelin, and brain iron.

Original languageEnglish (US)
Pages (from-to)122-125
Number of pages4
JournalAlzheimer's and Dementia
Volume3
Issue number2
DOIs
StatePublished - Apr 1 2007
Externally publishedYes

Keywords

  • Aging
  • Alzheimer's disease
  • Amyloid
  • Degeneration
  • Dementia
  • Iron
  • Medications
  • Myelin
  • Oligodendrocyte
  • PIB
  • Prevention
  • Treatment
  • White matter

ASJC Scopus subject areas

  • Epidemiology
  • Health Policy
  • Developmental Neuroscience
  • Clinical Neurology
  • Geriatrics and Gerontology
  • Psychiatry and Mental health
  • Cellular and Molecular Neuroscience

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