Heart failure & cardiomyopathies
Big tau aggregation disrupts microtubule tyrosination and causes myocardial diastolic dysfunction: from discovery to therapy
An erratum to this article was published (Eur Heart J, 14 Sep 2023 ↗)
Authors' conclusion
The study presents new mechanistic evidence and potential treatment for the brain-heart tauopathy axis in myocardial and brain degenerative diseases and ageing.
Study context
- Population
- Mouse model of tauopathy; human myocardial and brain tissue from patients with heart failure (HF), Alzheimer's disease (AD) and controls
Main finding
As reported in the abstract
- Tau is expressed in normal and diseased human hearts
- Main cardiac isoform is high-molecular-weight (HMW) (big) tau; hyperphosphorylated tau segregates in aggregates in HF and AD hearts
- Tauopathy phenotype in human myocardium is diastolic dysfunction
- Loss of tyrosinated microtubules emerged as a potential mechanism of myocardial tauopathy
- Monoclonal anti-tau antibody therapy improved myocardial function and clearance of toxic aggregates in mice
Original publication
Big tau aggregation disrupts microtubule tyrosination and causes myocardial diastolic dysfunction: from discovery to therapy. Eur Heart J. Published 1 May 2023. doi:10.
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