Alzheimer's Disease (Morbus Alzheimer): Pathophysiological Mechanisms and Breakthroughs in Disease-Modifying Therapeutics

This scientific article presents a comprehensive study on the pathophysiological cascades of Alzheimer's disease (Morbus Alzheimer) and the revolutionary paradigm shift in its pharmacological treatment. For decades, therapeutic options were restricted to symptomatic management via acetylcholinesterase inhibitors and NMDA receptor antagonists. However, recent scientific advances have led to the regulatory approval of novel disease-modifying therapies (DMTs), specifically monoclonal antibodies including Lecanemab (Leqembi®) and Donanemab (Kisunla®). These targeted biological agents remove extracellular neurotoxic amyloid-beta (Aβ) protofibrils and mature plaques, resulting in a clinically meaningful ~30% deceleration of cognitive and functional decline in early-stage patients. Furthermore, this paper highlights the biomarker role of intracellular hyperphosphorylated Tau protein (Proteinum Tau) and the clinical utility of ultra-sensitive plasma biomarkers (plasma p-tau217) for non-invasive early diagnostics.