All the Tau We Cannot See.
review · Level V
Where this comes from
- Record sourced from PubMed, PMID 36378913.
- Also identified by DOI 10.1146/annurev-med-042921-023749 and PMC identifier 11783578.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
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.
Medical subject headings
- tau Proteins
- Alzheimer Disease