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Basic Science and Pathogenesis.

Ai Liu1

  • 1McGill University, Montreal, QC, Canada.

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Pathological tau accumulation in Alzheimer's disease causes axonal damage, leading to myelin loss. While oligodendrocyte progenitor cells attempt remyelination, ongoing axonal degeneration hinders repair in this rat model.

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Area of Science:

  • Neuroscience
  • Pathology
  • Molecular Biology

Background:

  • Alzheimer's disease (AD) impacts both grey and white matter, causing axonal degeneration, demyelination, and glial issues.
  • Pathological hyperphosphorylated tau (p-Tau) is implicated in neurodegeneration.
  • Investigating p-Tau's role in axonal damage and myelin dynamics is crucial for understanding AD progression.

Purpose of the Study:

  • To investigate the impact of pathological hyperphosphorylated tau (p-Tau) on axonal damage.
  • To examine the effects of p-Tau on demyelination and remyelination processes.
  • To utilize an in vivo Alzheimer's-like tauopathy rat model.

Main Methods:

  • Generated McGill-R955-hTau transgenic (Tg) rats with P301S tau mutation.
  • Assessed cognitive function via behavioral testing.
  • Mapped tau expression, analyzed axonal damage, myelin pathology (electron microscopy), and oligodendrocyte markers (immunohistochemistry).

Main Results:

  • Tg rats showed age-dependent p-Tau increase, spreading to white matter, causing cognitive decline, neurodegeneration, axon, and myelin loss.
  • Ultrastructural analysis revealed extensive axonal and myelin degeneration.
  • Oligodendrocyte progenitor cells (OPCs) differentiated more efficiently in Tg rats, but remyelination failed due to increased axonal degeneration.

Conclusions:

  • Axonal damage from tau accumulation and glial phagocytosis leads to myelin pathology.
  • Demyelination may stimulate OPC differentiation for remyelination.
  • However, persistent axonal degeneration impedes successful myelin repair in this model.