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An astrocyte BMAL1-BAG3 axis protects against alpha-synuclein and tau pathology
A protective interaction in support cells helps prevent harmful protein build-up linked to brain diseases
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Abstract
Global post-natal deletion of Bmal1 in mice suppresses both tau and alpha-synuclein aggregation.
- Deletion of Bmal1 in mouse models of tauopathy and alpha-synucleinopathy reduces related pathology.
- Astrocyte-specific deletion of Bmal1 prevents both alpha-synuclein and tau pathology.
- Astrocyte Bmal1 deletion activates astrocytes and increases the expression of Bag3, essential for cellular cleanup processes.
- The deletion enhances the clearance of alpha-synuclein and tau proteins in a Bag3-dependent manner.
- In humans, increased levels of BAG3 are found in Alzheimer’s disease patients and in disease-associated astrocytes.
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