In Alzheimer’s patients, three dominant pools of amyloid-beta (Aβ) species have been identified: Aβ monomers, Aβ oligomers (Aβo) and fibrillar Aβ aggregates (plaques). The most prevalent species Aβ monomers and Aβ plaques, which are several orders of magnitude more prevalent in the brain have been the focus of Alzheimers’s drug development efforts during the past decade.

Based on seminal research pioneered by our founders, our drug discovery efforts have focused on targeting the far less abundant Aβo, which impair synaptic function, induce tau hyperphosphorylation and exacerbate inflammatory processes early in the disease process. Overwhelming scientific evidence now indicates that Aβo are the most toxic form of amyloid, causing acute synaptic toxicity to neurons, leading to the memory and cognitive impairment and chronic neurodegeneration that constitute the hallmark of Alzheimer’s disease.

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