Alzheimer's disease (AD) is the most common cause of progressive dementia in the 
elderly. It is characterized by a progressive and irreversible loss of cognitive 
abilities and formation of senile plaques, composed mainly of amyloid β (Aβ), 
and neurofibrillary tangles (NFTs), composed of tau protein, in the hippocampus 
and cortex of afflicted humans. In brains of AD patients the metabolism of Aβ is 
dysregulated, which leads to the accumulation and aggregation of Aβ. Metabolism 
of Aβ and tau proteins is crucially influenced by autophagy. Autophagy is a 
lysosome-dependent, homeostatic process, in which organelles and proteins are 
degraded and recycled into energy. Thus, dysfunction of autophagy is suggested 
to lead to the accretion of noxious proteins in the AD brain. In the present 
review, we describe the process of autophagy and its importance in AD. 
Additionally, we discuss mechanisms and genes linking autophagy and AD, i.e., 
the mTOR pathway, neuroinflammation, endocannabinoid system, ATG7, BCL2, BECN1, 
CDK5, CLU, CTSD, FOXO1, GFAP, ITPR1, MAPT, PSEN1, SNCA, UBQLN1, and UCHL1. We 
also present pharmacological agents acting via modulation of autophagy that may 
show promise in AD therapy. This review updates our knowledge on autophagy 
mechanisms proposing novel therapeutic targets for the treatment of AD.