Toxic Tau Aggregation in AD

Alzheimer’s disease (AD) is a neurodegenerative disorder that is caused by multiple factors, has a complicated physiopathology, and the causes of its onset are not well understood. An increasing body of clinical and experimental evidence points to a possible causal role of tau protein detachment from microtubules followed by tau aggregation in Alzheimer’s disease. This chapter provides a summary of what is currently known about how the tau protein becomes hyperphosphorylated, aggregated, and then transformed into a neurotoxic protein to trigger the primary pathophysiological mechanisms and anatomical changes in the brains of Alzheimer’s disease patients, as well as the connection between tau and amyloid beta (Aβ) and different AD biomarkers. Additionally, neurobiological processes that may be shared by different tauopathies and AD are investigated in this chapter. Emerging insights regarding the role of tau and its dysfunction in altering neuronal cascades and neuroplasticity and, as a result, initiating brain pathology in addition to tau-based immunotherapy are also discussed in this chapter.