RESEARCH ARTICLE The expression of apoptos

Full list of author information is available at the end of the articleBackground Alzheimer’s disease (AD) is an age-related neurodegenera-tive disorder, histologically characterized by the extracellu-lar deposition of amyloid β peptides (Aβ) and the intracellular accumulation of hyperphosphorylated tau. Numerous in vitro and in vivo studies have provided evidence for a key role of Aβ in AD [1,2]. Aβ-associated neurodegeneration involves cerebral cell death, but the underlying mechanisms remain largely unknown. Animal models of AD offer a unique opportunity to study the mechanisms involved in AD-related neurodegeneration, particularly the contribution of specific types of cell death during neuronal demise. Although neuronal death cannot be reproduced in all mouse models of AD, brain regions of some transgenic mice (e.g. PS1xAPP and TgCRND8) have been reported to demonstrate an age-dependent vulnerability, with the cortex and hippocampus being affected the earliest [3-5]. Neurodegeneration in age-associated dementia of the AD type is thought to involve neuronal cell loss by programmed cell death (PCD) [6,7]. Various caspases have been recognized as important mediators of neuronal PCD in AD [8] by classical caspase-dependent apoptosis