As the most common age-related neurodegenerative
disorder, Alzheimer’s disease (AD) currently affects 20–
30 million individuals worldwide [1]. The brain pathology
in AD that ultimately leads to cognitive decline and profound
dementia is characterized by extensive neuronal
loss, the formation of neurofibrillary tangles and the extracellular
deposition of amyloid-b (Ab; see Glossary) plaques
in susceptible regions of the brain, accompanied by a
chronic inflammatory response and extensive oxidative
damage most probably as a reaction to amyloid deposition
[2]. Although the initiating cause of idiopathic AD is still
unknown, the amyloid cascade hypothesis states that the
aberrant production of Ab is a causative agent in the
pathogenesis in AD [2], and that selectively lowering production
of the Ab(1–42) peptide (Ab42) could be a promising
strategy for prevention or therapy of this disease [3].