Mechanism of Action
In neurodegeneration, the brain faces an assault: abnormal protein aggregates like tau and alpha-synuclein accumulate, and inflammation injures the delicate neuros.
Our discovery program for Parkinson's disease and tauopathies targets these phenomena by activating processes to reduce the buildup of protein and enhance the clearance of existing aggregates. At the same time, our approach tackles neuroinflammation, creating a healthier environment for neurons to thrive. By preserving neuronal vitality, we aim to slow or even stop the progression of these debilitating diseases.
PREP/PP2A interaction modulation
Protein phosphatase 2a is a critical regulator of protein dephosphorylation in the brain as well as central regulator of autophagy. Lowered levels if PP2A and activity is seen in Alzheimer’s disease and other tauopathies.
Increases autophagy and degradation of tau and α-syn
Autophagy boosts the clearance of neurotoxic tau and α-syn aggregates that accumulate in tauopathies and Parkinson’s.
Dephosphorylates tau and α-syn
Autophagy boosts the clearance of neurotoxic tau and α-syn aggregates that accumulate in tauopathies and Parkinson’s.
Reduces oxidative stress
PP2A activation has direct downstream effects in reducing oxidative stress.
Reduces glial cell activation
PP2A activation dampens neuroinflammatory response thus having neuroprotective effects.
