A protective interaction in support cells helps prevent harmful protein build-up linked to brain diseases

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.

Simplified