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Related Experiment Videos

[Abeta, tau and alpha-synuclein and glial cells].

Haruhiko Akiyama1

  • 1Tokyo Institute of Psychiatry, Japan. akiyama@prit.go.jp

Nihon Shinkei Seishin Yakurigaku Zasshi = Japanese Journal of Psychopharmacology
|April 28, 2006
PubMed
Summary
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Abnormal protein accumulation, including amyloid beta-protein, tau, and alpha-synuclein, drives neurodegenerative diseases. Glial cells play a key role in these proteinopathies and neuronal degeneration.

Area of Science:

  • Neurobiology
  • Cellular pathology

Context:

  • Neurodegenerative diseases like Alzheimer's and Parkinson's are linked to abnormal protein buildup in the brain.
  • Key proteins involved include amyloid beta-protein (Abeta), tau, and alpha-synuclein, which are central to disease pathogenesis.

Purpose:

  • To elucidate the roles of glial cells (microglia and astrocytes) in the accumulation and clearance of pathogenic proteins.
  • To explore how glial cells contribute to neuroinflammation and neuronal degeneration in proteinopathies.

Summary:

  • Microglia and astrocytes clear soluble Abeta, but clearance of insoluble Abeta by microglia triggers neuroinflammation.
  • Tau accumulates in astrocytes and oligodendrocytes in various forms (e.g., tuft-shaped astrocytes, coiled bodies), characteristic of specific tauopathies.
  • Alpha-synuclein accumulation in oligodendrocytes (glial cytoplasmic inclusions) is diagnostic for multiple system atrophy.

Related Experiment Videos

  • Transgenic models show that glial cells accumulating tau or alpha-synuclein can lead to neuronal degeneration, highlighting glial pathogenic roles.

    • Impact:

    • Understanding glial cell involvement in protein accumulation and neuroinflammation is crucial for developing targeted therapies for neurodegenerative diseases.
    • This research supports the concept that abnormal glial cells actively contribute to neuronal damage in conditions like Alzheimer's, Parkinson's, and tauopathies.