Molecular Mechanisms of FDA-Approved Drugs for the Treatment of Alzheimer's Disease: A Comprehensive Review

Abstract

Alzheimer’s disease (AD) is characterized by progressive degeneration of neurons. It is a complex and multifactorial disorder. Symptomatic modulation of neurotransmitter pathways and disease-modifying treatments are the current therapeutic approaches in molecular medicine. The efficacy of Food and Drug Administration (FDA)-approved medications for AD has improved over time. Among the classes of drugs, cholinesterase inhibitors (ChEIs) and N-methyl-D-aspartate receptor (NMDAR) antagonists are used for symptom management. The combination of these treatments improves understanding about neurotransmitter abnormalities in AD. Although their processes differ, they complement each other in terms of effectiveness. The mechanistic evidence remains underexplored for these interactions. With time, treatment advancement
introduced anti-amyloid monoclonal antibodies. This shifted the therapeutic focus toward targeted intervention. These drugs selectively target pathogenic amyloid plaques and clear them from brain tissues, which further clears amyloid in the bloodstream. The immune-mediated process provided by this class of drugs differs in both efficacy and downstream biological pathways. These steps in the mechanism are critical; emerging observations need to inquire regarding their treatment specificity, biological variability, and safety mechanisms in neural and cellular safety signaling pathways. In this review, therapeutic classes with distinct mechanisms are explored at the molecular level, where immune activation, aggregated protein clearance, and symptomatic modulation intersect. The review discusses a combination of these molecular-level understandings of AD pathology and how treatments interact with biological systems across conventional and innovative therapeutic options.