Alzheimer’s Disease
Alzheimer’s causes a disruption to the connections between neurons in the brain, which effects a person’s cognitive abilities, including learning and memory. Symptomatic treatments to improve cognition in Alzheimer’s are unsatisfactory and there is no FDA-approved drug that results in sustained improvement in cognitive function.
Many theories have been proposed on the cause and mechanism of disease progression in Alzheimer’s and treatment has been focused on reducing the build up of amyloid beta (Aβ) and tau protein, which are strongly associated with neurodegeneration in Alzheimer’s patients. The aim of these treatments has been to delay or reverse the worsening of symptoms. Studies in animals has suggested that degrading or reducing the build up of these proteins improves Alzheimer’s symptoms. However, the same has not been shown in humans.
Alzheimer’s Disease and NVG-291
NervGen’s goal is to repair the damage seen in Alzheimer’s patients and improve cognitive function. A build up of CSPGs has been shown in the brains of patients with Alzheimer’s (Howell et al., 2015) and preclinical studies have demonstrated that breaking down CSPGs improves Alzheimer’s symptoms (Yang et al., 2015; Vegh et al., 2014). It has also been shown that removing the cellular receptor that CSPGs bind to, protein tyrosine phosphatase sigma (PTPσ), improves cognitive function in Alzheimer’s models (Gu et al., 2016). Because NVG-291-R relieves the inhibitory effects of CSPGs in animal models, it is expected that NVG-291 may improve the function of neurons and strengthen their connections, which may improve cognition.
A list of select scientific publications that give an overview of the robust effects of NVG-291-R seen in animal models is provided in our list of Journals & Publications.
