Abstract
Alzheimer's disease (AD) is the most common cause of dementia, which is characterized by a progressive neurodegenerative disorder that is extremely difficult to treat and severely reduces quality of life. Amyloid beta (Aβ) has been the primary target of experimental therapies owing to the neurotoxicity of Aβ and the brain Aβ load detected in humans by amyloid positron emission tomography (PET) imaging. Recently completed phase 2 and 3 trials of third-generation anti-amyloid immunotherapies indicated clinical efficacy in significantly reducing brain Aβ load and inhibiting the progression of cognitive decline. Anti-amyloid immunotherapies are the first effective disease-modifying therapies for AD, and aducanumab and lecanemab were recently approved through the US Food and Drug Administration's accelerated approval pathway. However, these therapies still exhibit insufficient clinical efficacy and are associated with amyloid-related imaging abnormalities. Further advances in the field of AD therapeutics are required to revolutionize clinical AD treatment, dementia care, and preventive cognitive healthcare.