Targeting Alzheimer's Disease: A Comprehensive Review of Current Drug Targets, Receptors, Enzymes, and Neurotransmitters

Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized by progressive cognitive decline and memory impairment. Despite extensive research, current therapeutic options remain limited, and there is no cure. Recent advancements have expanded the understanding of key molecular mechanisms underlying AD pathogenesis, paving the way for novel therapeutic approaches. This review aims to provide a comprehensive analysis of the current drug targets for AD, focusing on various receptors, enzymes, and neurotransmitters involved in disease progression. The amyloid-beta (A?) cascade, tau protein hyperphosphorylation, synaptic dysfunction, oxidative stress, neuroinflammation, and impaired neurotransmission represent major pathological hallmarks of AD. Therapeutic strategies have been developed to target these processes, including ?-secretase (BACE) and ?-secretase inhibitors for reducing amyloid deposition, tau kinase inhibitors to prevent tau hyperphosphorylation, and cholinesterase inhibitors to enhance cholinergic neurotransmission. Additionally, drugs targeting N-methyl-D-aspartate (NMDA) receptors aim to prevent excitotoxicity. Emerging therapies focus on modulating neuroinflammatory pathways, targeting microglial activation, and blocking pro-inflammatory cytokines. Receptors such as nicotinic acetylcholine receptors (nAChRs), GABA receptors, serotonin receptors, and muscarinic receptors are explored for their roles in maintaining neurotransmitter balance and neuroprotection. This review will explore these drug targets in detail, discussing both established and experimental therapeutic strategies. We will provide illustrative diagrams and tables to highlight the receptor-ligand interactions, signaling pathways, and the role of various enzymes and neurotransmitters in the progression of AD. Additionally, we will discuss the clinical efficacy and challenges of current and potential