Alzheimer’s disease is characterized by neurofibrillary degeneration involving abnormal hyperphosphorylation of microtubule-associated protein tau and β-amyloidosis of the brain. There is increasing evidence that inhibition or removal of β-amyloid alone might not be sufficient to treat or slow the progression of Alzheimer’s disease. The objective of this symposium is to discuss and evaluate the rationale and therapeutic approaches that would inhibit tau pathology.

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