ABOUT NEUROSN

NeuroSn, Inc., is developing therapies for patients with Alzheimer's disease and other inflammatory-mediated dementias.

Alzheimer’s disease, our primary target, exhibits hallmark neuropathological features including the deposition of aggregates of insoluble amyloid-β peptides and neurofibrillary tangles. These pathological protein deposits had been assumed to be the primary cause of Alzheimer’s, and were extensively targeted in attempts to develop an effective disease-modifying therapy with little clinical success to date. There is a significant role of inflammation in the pathogenesis of Alzheimer's disease, and the activation of microglia contributes to an increase of amyloid-β and tau phosphorylation. Inactivating pro-inflammatory microglia could be beneficial in treating Alzheimer's disease.

Microglia are resident brain cells that normally exist in an inactive state. However, in the early stages of Alzheimer’s after stimulation by pathogens or injury, the microglia become activated, initially phagocytosing amyloid-β until their capacity is reached. These engorged, aged microglia then contribute to direct neuronal injury by perpetuating a mixture of the classical activation pathway and an exacerbated increase of alternative activation which leads to irreparable damage and persistent neurodegeneration. 

Our Alzheimer’s therapy focuses on this inflammatory pathway by eliminating the chronic pro-inflammatory microglia that exacerbate neuroinflammation and induce neuronal death.