Alzheimer’s Disease (AD) is an age-dependent neurodegenerative disorder, the most common
type of dementia that is clinically characterized by the presence of beta-amyloid (Aβ) extracellularly and
intraneuronal tau protein tangles that eventually leads to the onset of memory and cognition impairment,
development of psychiatric symptoms and behavioral disorders that affect basic daily activities. Current
treatment approved by the U.S Food and Drug Administration (FDA) for AD is mainly focused on the
symptoms but not on the pathogenesis of the disease. Recently, receptor-interacting protein kinase 1
(RIPK1) has been identified as a key component in the pathogenesis of AD through necroptosis. Furthermore,
genetic and pharmacological suppression of RIPK1 has been shown to revert the phenotype of
AD and its mediating pathway is yet to be deciphered. This review is aimed to provide an overview of
the pathogenesis and current treatment of AD with the involvement of autophagy as well as providing a
novel insight into RIPK1 in reverting the progression of AD, probably through an autophagy machinery.
An RNA-dependent protein kinase is involved in tunicamycin-induced apoptosis and Alzheimer's disease