Targeting Substance P Pathway as an Emerging Novel Therapeutic Mechanism for Modulating Amyloid Beta in APP/PS1 Mouse Model

Neurodegeneration associated with Alzheimer’s disease (AD) is well established to be mediated by amyloid β (Aβ) plaques and neurofibrillary tangles (NFTs) of Tau protein in the brain. However, there are a multitude of underlying processes that individually contribute to the development of these aberrant Aβ aggregations and NFTs over time that are still being elucidated. The substance P/neurokinin‐1 receptor signaling pathways play an important role in regulating neuroinflammation and have recently been demonstrated to also influence mechanisms responsible for Aβ amyloidogenesis and toxicity1,2,3. Accordingly, HT‐ALZ is under development as a novel AD therapeutic to target the SP/NK1R pathway.