Neurones in the brain produce beta -amyloid (A beta) fragments from a large
r precursor molecule termed the amyloid precursor protein (APP). When relea
sed from the cell. these protein fragments may accumulate in extracellular
amyloid plaques and consequently hasten the onset and progression of Alzhei
mer's disease (AD). beta -Amyloid fragments are generated through the actio
n of specific proteases within the cell. Two of these enzymes, beta- and ga
mma -secretase, are particularly important in the formation of A beta as th
ey cleave within the APP protein to give rise to the N-terminal and C-termi
nal ends of the A beta fragment, respectively. Consequently, many researche
rs are investigating therapeutic approaches that inhibit either beta- or ga
mma -secretase activity, with the ultimate goal of limiting A beta producti
on. 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 plaqu
es may be an effective treatment for AD.