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Basic Science and Pathogenesis.

Magdalena M Bolsinger1, Bruno Ghirotto1, Denise Balta1

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Summary
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Astrocytes clear alpha-synuclein (αS) via lysosomes, but pathology impairs this function. However, astrocyte lysosomes show remarkable resilience and can recover, suggesting therapeutic potential for neurodegenerative diseases like DLB.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Astrocytes are crucial for clearing alpha-synuclein (αS), a protein linked to neurodegenerative diseases like dementia with Lewy bodies (DLB) and Parkinson's disease.
  • Lysosomes are key to degrading aggregated proteins, but their response to αS pathology in astrocytes is not well understood.

Purpose of the Study:

  • To investigate the mechanisms of astrocytic lysosomal responses to αS pathology.
  • To assess the capacity of astrocytes to internalize and degrade fibrillar αS.

Main Methods:

  • Analysis of lysosomal systems in primary wild-type astrocytes, iPSC-derived astrocytes, and an αS-overexpressing mouse model.
  • Assessment of key lysosomal enzymes (e.g., GBA, cathepsins) and proteins (e.g., LAMP-2, LIMP-2) using Western blotting, immunofluorescence, and mass spectrometry.
  • Evaluation of astrocyte internalization and degradation of fibrillar αS.

Main Results:

  • Fibrillar αS induced lysosomal dysfunction in primary astrocytes, with reversible changes in enzyme activity.
  • iPSC-derived astrocytes effectively internalized and degraded αS fibrils, enhancing lysosomal enzyme activity.
  • Astrocytes from an αS-overexpressing model showed impaired lysosomal function but recovered after αS removal.

Conclusions:

  • Fibrillar αS causes time-dependent changes in astrocytic lysosomal function, which are largely reversible.
  • Astrocytes possess a significant capacity to manage and degrade exogenous pathological αS.
  • Targeting astrocytic lysosomal pathways may offer a therapeutic strategy for α-synucleinopathies.