In Alzheimer’s disease, neuronal hyperactivity is one of the earliest pathological alterations in Alzheimer’s disease contributing to detrimental calcium dyshomeostasis. reMYND’s lead ReS3-T program targets a central regulator of neuronal activity to restrain neuronal hyperactivity in a disease context. As a result ReS3-T treatment counters Tau and Abeta driven toxicity, restores neuronal hyperactivity and is neuroprotective in preclinical models of Alzheimer’s.
Given the mechanism and its efficacy profile in Alzheimer’s, ReS3-T is expected to counter also epileptogenesis and to have neuroprotective activity in epilepsy without the severe side effects of currently existing symptomatic treatments.
reMYND is researching and developing this program together with CD3.