Targeting Aβ protein in Alzheimer’s Disease

Alzheimer's disease (AD) is one of the most common causes of dementia in the society. Recent reports suggest that > 4.7 million people of ≧ 65 years of age are living with AD in the USA. AD is predicted to affect one in 85 people globally by 2050. The malfunctioning and gradual death of neurons in the disease results in loss of memory and cognitive functions. The disease is characterized by accelerated accumulation of amyloid β (Aβ) plaque around neurons and hyperphosphorylated microtubule associated tau protein in the form of neurofibrillary tangles within the cells. In this review, we have described and discussed the recent focus on therapeutic interventions targeting at various Aβ-associated pathological mechanisms of AD and experimental strategies focusing on Aβ which aim to decrease the production of the protein, prevent its aggregation or increase the removal of it from the brain. The β secretase is (the enzyme that initiates the generation of Aβ) an attractive drug target for lowering cerebral levels of APP for the treatment of AD. It was noted that that Aβ represents a potent molecular target for pharmacological manipulation to perhaps prevent the onset and progression of Alzheimer's disease.