Drug development against dementia based on understanding of molecular and cellular pathogenesis

Abstract

Pathological and molecular genetic analyses have revealed that amyloid-β peptide and tau protein are involved in the pathogenesis of Alzheimer disease (AD). Moreover, identification of cerebrospinal biomarker, advances in brain imaging and results of observational cohort studies indicate that AD is a chronic disease with abnormal protein metabolism in the brain. Current approaches targeting pathogenic molecules for AD have been developed as preventive medicine. In addition, abnormal protein aggregation is now recognized as a common pathological feature of neurodegenerative diseases that cause dementia. Thus, cellular pathologies in the brain along with the deposition of aggregated protein are highlighted as novel therapeutic key targets in the drug development.