This technology is a biologic platform that enhances SUMO2 conjugation to preserve or restore synaptic function and memory in Alzheimer’s disease (AD) without altering amyloid burden.
Current therapies for Alzheimer’s disease (AD) primarily aim to reduce amyloid-β plaques and tau tangle formation or enhance their clearance; however, these approaches have shown limited success in reversing cognitive decline associated with AD. Many patients continue to experience progressive dementia in the form of synaptic dysfunction and memory loss, even as the amyloid burden is reduced. There remains a critical need for therapies that directly preserve or restore synaptic function, particularly therapies that are effective in later stages of disease.
This technology is a therapeutic platform that utilizes a modified small ubiquitin modifier 2 (SUMO2) peptide to prevent and reverse synapse loss and cognitive deficits associated with Alzheimer’s disease (AD). SUMO2 conjugation plays a critical role in long-term potentiation, a synaptic mechanism fundamental to learning and memory. Through systemic administration of a recombinant biologic, SUMO2 conjugation is selectively elevated in the brain without altering amyloid production or clearance. The biologic is designed for efficient brain penetration and localizes to synaptic compartments, where it promotes stability and function by modulating protein interactions and stress responses linked to neurodegeneration.
This technology has been validated in vivo using AD mouse models.
Luana Fioriti
Paul Fraser, Ph.D.
Patent Issued (WO/2024/192296)
IR CU23265
Licensing Contact: Jerry Kokoshka