Restoring the acidifying function of lysosomes for Alzheimer's disease therapy

Abstract

Alzheimers disease, abbreviated as AD, is a clinical syndrome that often occurs in the elderly, characterized by progressive deterioration of memory and cognitive function. The disease usually manifests gradually, following a slow and irreversible progression. It leads to brain atrophy and eventual cell death. Recent research suggests that Alzheimers disease may result from nerve cell death followed by the appearance of extracellular amyloid plaques. This study will focus on lysosomal acidification disorders, which lead to lysosomal rupture and subsequent cell death. The abnormal acidic environment in lysosomes is mainly due to the increase in pH value and the loss of activity of V-ATPase. This work will investigate the potential of pharmacological agents and nanoparticles to restore lysosomal acidification by enhancing V-ATPase activity and lowering pH levels. The research demonstrates that nanoparticle-based and pharmacological methods hold promise for addressing the dysfunction in lysosomal acidification, a key issue in Alzheimers disease.