The Interplay Between Accumulation of Amyloid-Beta and Tau Proteins, PANoptosis, and Inflammation in Alzheimer’s Disease

Alzheimer’s disease (AD) is a common progressive neurodegenerative disorder, and the vast majority of cases occur in elderly patients. Recently, the accumulation of Aβ and tau proteins has drawn considerable attention in AD research. This review explores the multifaceted interactions between these proteins and their contribution to the pathological landscape of AD, encompassing synaptic dysfunction, neuroinflammation, and PANoptosis. PANoptosis is a collective term for programmed cell death (PCD) modalities that encompass elements of apoptosis, pyroptosis, and necroptosis. The accumulation of Aβ peptides and tau proteins, along with the immune response in brain cells, may trigger PANoptosis, thus advancing the progression of the disease. Recent advancements in molecular imaging and genetics have provided deeper insights into the interactions between Aβ peptides, tau proteins, and the immune response. The review also discusses the role of mitochondrial dysregulation in AD. The exploration of the interplay between neurodegeneration, immune responses, and cell death offers promising avenues for the development of innovative treatments.