Alzheimer's disease (AD) is a neurodegenerative disease characterized by cognitive impairment so widespread that it interferes with a person's ability to complete daily activities. AD is becoming increasingly common, and it is estimated that the number of patients will reach 152 million by 2050. Current treatment options for AD are symptomatic and have modest benefits. Therefore, considering the human, social, and economic burden of the disease, the development of drugs with the potential to alter disease progression has become a global priority. In this review, the molecular mechanisms involved in the pathology of AD were evaluated as therapeutic targets. The main aim of the review is to focus on new knowledge about mitochondrial dysfunction, oxidative stress, and neuronal transmission in AD, as well as a range of cellular signaling mechanisms and associated treatments. Important molecular interactions leading to AD were described in amyloid cascade and in tau protein function, oxidative stress, mitochondrial dysfunction, cholinergic and glutamatergic neurotransmission, cAMP-regulatory element-binding protein (CREB), the silent mating type information regulation 2 homolog 1 (SIRT-1), neuroinflammation (glial cells), and synaptic alterations. This review summarizes recent experimental and clinical research in AD pathology and analyzes the potential of therapeutic applications based on molecular disease mechanisms.
Keywords: Alzheimer's disease; acetylcholine; amyloid; synaptic transmission.
© 2022 Société Française de Pharmacologie et de Thérapeutique. Published by John Wiley & Sons Ltd.