Background: Cellular prion protein PrPC acts as a high affinity receptor for Aβ-oligomers and is required for Aβ-oligomer-induced synaptic dysfunction in vitro and in vivo. Signal transduction downstream of Aβo/PrPC involves mGluR5, Fyn and Pyk2.

In an AD Tg mouse model an infusion of the anti-PrPC mAb produces a significant behavioral rescue in the setting of advanced disease, even with a relatively short treatment regiment (Fig.1).

Indications: Alzheimer’s Disease; prion-related diseases (CJD, etc).

References: Heiss et al. (2016) Cereb Cortex; Salazar et al. (2017) Biochem Biophys Res Comm.

IP status: Issued patent US 9217036; option to commercially-developed human mAbs.

Lead Innovator: Stephen M. Strittmatter, M.D., Ph.D.