Understanding the Potential Targets of Alzheimer’s Disease

Alzheimer’s disease (AD) is a protein-prominent and chronic neurodegenerative disorder. The crucial pathogenic events in AD include Amyloid-β plaque aggregation, neurofibrillary tangles (tau hyperphosphorylation), neuroinflammation, oxidative stress, synaptic dysfunction, and mitochondrial dysfunction. All these factors eventually lead to neurodegeneration (neuronal death). Due to its complex pathophysiology and multi-factorial nature, researchers across the world are experiencing ceaseless and tedious journey to identify potential targets for the treatment of AD. One possible reason behind the failure of many anti-AD therapies clinically is cross-talk and interaction between two or more pathogenic events of AD. In this context, there is a need to identify potential targets that mainly focus on pathogenic mechanisms and thereby slow down the process of neurodegeneration in AD. In connection to this, some of the potential targets that aim at neurodegeneration include beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), fyn kinase, mitochondrial regulators, purinergic receptors, cannabinoid receptor 2, renin angiotensin system (RAS), sigma receptor, ApoE4, and enzymes such as glycogen synthase kinase-3, lipoxygenases, secretases, caspases, and sirtuins. The current chapter focuses on some of the above-mentioned potential targets, their involvement in AD pathogenesis, the mechanism of targeting pathogenic factors, and their therapeutic efficacy in preclinical and clinical studies.