Tau Pathology Without A β

Alzheimer disease (AD) is characterized by accumulation of amyloid- β (Aβ) plaques and tau neurofibrillary tangles that can be identified at autopsy or during life with fluid or imaging biomarkers. The presence of Aβ accumulation is an early event that precedes cognitive impairment by at least a decade and, based on the National Institute on Aging–Alzheimer’s Association Research Framework, defines whether an individual is on the AD pathway. The pathologic spread of tau aggregations throughout the brain appears to be triggered by Aβ, a sequence supported by the observation that abnormal tau, especially when present beyond the medial temporal lobe (MTL) , is uncommon in the absence of abnormal Aβ. Within the MTL, however, tau aggregation is nearly universal by age 80 years, regardless of Aβ status. Furthermore, tau aggregation composed of different tau protein constituents is a defining feature of other neurodegenerative diseases that do not invo lve abnormal Aβ accumulation, such as Pick disease, progressive supranuclear palsy, and chronic traumatic encephalopathy.
Source: JAMA Neurology - Category: Neurology Source Type: research