Aging compromises oligodendrocyte precursor cell maturation and efficient remyelination in the monkey brain

Christina Dimovasili1, Ashley E Fair2, Isabella R Garza2

  • 1Laboratory for Cognitive Neurobiology, Department of Anatomy & Neurobiology, Boston University School of Medicine, Boston, MA, USA. cdimovasili@gmail.com.

Geroscience
|August 5, 2022
PubMed

Insights

Cognitive decline in aging is linked to myelin damage and reduced repair. Older monkeys show fewer new myelin-producing cells and impaired differentiation, hindering brain repair.

Area of Science:

  • Neuroscience
  • Aging Research
  • Cell Biology

Background:

  • Age-associated cognitive decline is common in healthy elderly individuals.
  • White matter loss and myelin damage correlate with cognitive decline, independent of neuron loss.
  • Myelin damage from oxidative stress is repaired by oligodendrocyte precursor cells (OPCs).

Purpose of the Study:

  • To investigate how aging affects the brain's capacity for myelin regeneration using a rhesus monkey model.
  • To identify age-related changes in oligodendrocyte precursor cells (OPCs) and mature oligodendrocytes.
  • To correlate myelin regeneration capacity with cognitive performance in aging.

Main Methods:

  • Utilized the rhesus monkey model of normal aging.
  • Examined the numbers of new BCAS1+ myelinating oligodendrocytes in aged subjects.
  • Assessed the proliferation and differentiation potential of OPCs, focusing on the transcription factor NKX2.2.
  • Measured RNA expression of myelin protein markers (MBP and PLP) in mature oligodendrocytes.

Main Results:

  • Older rhesus monkeys exhibited reduced numbers of new myelinating oligodendrocytes, associated with poorer cognitive function.
  • OPC proliferation was not limited in aged subjects; however, the transcription factor NKX2.2 was significantly decreased.
  • Mature oligodendrocytes in aged brains showed reduced expression of myelin proteins MBP and PLP.
  • These findings indicate an impaired capacity for remyelination in the aging brain.

Conclusions:

  • Aging impairs the brain's ability to regenerate myelin due to reduced differentiation potential of OPCs and decreased myelin production by mature oligodendrocytes.
  • The decline in myelin regeneration capacity contributes to age-associated cognitive decline.
  • Targeting OPC differentiation and myelin production may offer therapeutic strategies for cognitive aging.