Alzheimer disease (AD) is defined pathologically and diagnostically defined by amyloid-β
senile plaques and neurofibrillary tangles (NFT) composed of tau. From the time of their
original description nearly a century ago, a major focus has been to understand the role that
these lesions play in the pathogenesis of the disease. The majority favors the notion that
these lesions cause the disease and therefore attempts at therapeutic intervention are
focused on preventing lesions formation. However, this rationale may be misguided since …