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forms of Aβ lead to Aβ-induced neuroinflammation as a key component of
Alzheimer’s disease pathology. In addition, ApoE function correlates with other
neuropathological changes in Alzheimer’s disease some of which are
Aβ-independent.
Our Work
We are
currently developing drug-like molecules that potentiate the expression and
function of ApoE via engagement of a novel biological target.
Increasing the
levels and function of ApoE aids in the clearance of Aβ from the CNS correcting
a key imbalance in the early stages of Alzheimer’s disease. Additionally, enhanced ApoE function may
ameliorate certain Aβ-independent neuropathological changes characteristic of
dementia.
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