Blocking amyloid-beta peptide aggregation
The triggers of Alzheimer’s disease progression are the amyloid-beta peptides (AB40 and AB42) being cleaved from the native human amyloid precursor protein (APP) by the BACE protease and g-secretase. Besides accumulating into amyloid fibrils and plaques within the brain, the misfolded and aggregated amyloid-beta peptides accumulate in neuronal synapses to initiate neurotoxicity and the formation of tau tangles inside of the neurons. The malfunction or death of many neurons affected by amyloid-beta peptide accumulation causes changes in one’s memory, behavior and ability to think clearly. In Alzheimer’s disease, these brain changes eventually impair an individual’s ability to carry out such basic bodily functions as walking and swallowing, and is ultimately fatal. ALZT-OP1, being developed by AZTherapies, is designed to prevent amyloid-beta peptide aggregation, thereby preventing them from accumulating in neuronal synapses. The drug-treated amyloid-beta peptides are then able to pass harmlessly into the bloodstream to be filtered out of the body. Multifunctional therapy with the ALZT-OP drugs will consistently prevent the low-level daily production of amyloid-beta peptides from triggering Alzheimer’s disease progression and suppress neuroinflammation associated with the disease.