β-amyloid therapies in Alzheimer's disease

Neurones in the brain produce beta -amyloid (A beta) fragments from a larger precursor molecule termed the amyloid precursor protein (APP). When released from the cell. these protein fragments may accumulate in extracellular amyloid plaques and consequently hasten the onset and progression of Alzheimer's disease (AD). beta -Amyloid fragments are generated through the action of specific proteases within the cell. Two of these enzymes, beta- and gamma -secretase, are particularly important in the formation of A beta as they cleave within the APP protein to give rise to the N-terminal and C-terminal ends of the A beta fragment, respectively. Consequently, many researchers are investigating therapeutic approaches that inhibit either beta- or gamma -secretase activity, with the ultimate goal of limiting A beta production. An alternative AD therapeutic approach that is being investigated is to employ anti-A beta antibodies to dissolve plaques that have already formed. Both of these approaches focus on the possibility that accrual of A beta leads to neuronal degeneration and cognitive impairment characterised by AD and test the hypothesis that. limiting A beta deposition in neuritic plaques may be an effective treatment for AD.