All the Tau We Cannot See
Year: 2022
Type: review
Abstract: Alzheimer's disease (AD) was described in 1906 as a dementing disease marked by the presence of two types of fibrillar aggregates in the brain: neurofibrillary tangles and senile plaques. The process of aggregation and formation of the aggregates has been a major focus of investigation ever since the discoveries that the tau protein is the predominant protein in tangles and amyloid β is the predominant protein in plaques. The idea that smaller, oligomeric species of amyloid may also be bioactive has now been clearly established. This review examines the possibility that soluble, nonfibrillar, bioactive forms of tau-the "tau we cannot see"-comprise a dominant driver of neurodegeneration in AD.
Source: Annual Review of Medicine
Author: Bradley Hyman
Institution: Massachusetts General Hospital
Language: English
Subfield: Physiology (medical)
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
Funder: National Institute on Aging
Awards: LRP1-tau interactions and Alzheimer Disease, Synergy between amyloid and tau in Alzheimer's Disease, Complexity and Heterogeneity of Alzheimer disease, Are multiple tau species toxic in Alzheimer's Disease?, LRP1-tau interactions and Alzheimer Disease, Massachusetts Alzheimer's Disease Research Center (MADRC)
OpenAlex ID: W4309087248