Currently 46,8 million people worldwide suffer from dementia, doubling every 20 years. Alzheimer’s disease (AD) is by far the most common dementia in late life with a prevalence of one in nine people with an age of 65 and older and is the 6th leading cause of death.
Pathologically the disease is characterized by the presence of amyloid aBeta plaques and fibrillary Tau tangles. Symptoms include memory loss and other cognitive tasks which severely disrupt daily life of patients and family members. This cognitive impairment results from synaptic loss, later on followed by neuronal degeneration in specific brain regions. Ca2+ dyshomeostasis is a pivotal process driving the loss of synaptic plasticity with as well aBeta as Tau pathology
Even though current therapeutics sell for 5 billion USD and are forecasted to grow to 11 billion USD by 2021 (CAGR 11%), no treatments are available that stop or even slow down disease progression. Existing therapies are all symptomatic, whereas most ongoing developments for causal remedies aimed to inhibit neuronal degeneration have had mixed results up to now.
reMYND’s lead ReS19-T program restores calcium dyshomeostasis in AD, a process central in the disease cascade leading to neuronal demise and build-up of plaques and tangles. By targeting the disease in its tracks ReS19-T mitigates neuronal loss and pathology but has also an immediate symptomatic benefit on synaptic plasticity, cognition and cerebrospinal biomarkers, allowing for a manageable clinical translatibility.
Currently the program is undergoing IND-enabling tox studies in order to start clinical studies.