Fig.1.

Presenilin-1 (PS-1) mutation leads to several changes in the cell due to improper cleavage of the amyloid-β protein precursor (AβPP). PS-1 mutation causes the improper cleavage of AβPP leading to aberrant forms of amyloid-β (Aβ) which occurs in both the cell and mitochondrial membrane. Accumulation of aberrant Aβ proteins form Aβ plaques which cause increased intracellular oxidative stress and influx of calcium ion. Both of these events lead to mitochondrial dysfunction which in turn increases oxidative stress and cellular damage.