Interlacing the relevance of caspase activation in the onset and progression of Alzheimer’s disease

Caspases, a family of cysteine proteases is a renowned regulator of apoptosis. Members of this family are responsible for the proteolytic dismantling of numerous cellular structures. Apart from apoptosis, caspases remarkably contribute to a diverse range of molecular processes. Being the imperative members of several cellular cascades their abnormal activation/deactivation has severe implications and also leads to various diseased conditions. Similar aberrant activation of caspases is one of the several causes of neuropathologies associated with Alzheimer’s disease (AD), a form of dementia severely affecting neuropsychiatric and cognitive functions. Emerging studies are providing deeper insights into the mechanisms of caspase action in the progression of AD. Current article is an attempt to review these studies and present the action mechanisms of different mammalian caspases in the advancement of AD associated neuropathologies. [Display omitted] •Amyloid plaques and neurofibrillary tangles are the leading pathologies associated with AD.•Different members of caspase family are activated in response to the primary AD pathologies.•Mammalian caspases exhibit a multifaceted role in the progression of AD.