Alzheimer's disease (AD) is associated with elevated levels of Amyloid-â peptide (Aâ), which acts as a pathological trigger culminating in neuronal death and dementia. A promising avenue for treating AD is in the use of selective and stable somatostatin receptor (SSTR) agonists, which may act to reduce Aâ through enhancement of enzymatic degradative processes. This research will evaluate our novel SSTR agonists as to their ability to mitigate Aâ concentrations in the brain in conjunction with learning and memory retention, using established models and assessments of AD pathology.