IMPACTS OF REDUCING β-AMYLOID PLAQUES IN PHARMACOLOGICAL TREATMENT WITH DONANEMAB IN ALZHEIMER'S DISEASE

Abstract

Alzheimer's disease (AD) is a progressive, irreversible neurodegenerative disease characterized by memory loss and cognitive function. Its pathophysiology involves the accumulation of beta-amyloid plaques and, in some cases, hyperphosphorylated tau protein in the synaptic cleft. Factors such as neuroinflammation and oxidative stress also contribute to its progression. This work examines the most recent therapy, Donanemab, a drug approved by ANVISA in April 2025, which acts on beta-amyloid degradation. Understanding these mechanisms is essential for developing strategies to slow disease progression and reduce neuronal damage