It has recently been shown that acetylation of soluble tau oligomers is increased in the brains of people with mild-to-moderate Alzheimer disease (AD). This study shows that, in a mouse model of AD and also in human AD, acetylation of tau at the K174 residue is a key pathological change that increases tau accumulation. In a mouse model of frontotemporal dementia, inhibition of tau acetylation reduced tau accumulation and behavioural deficits, suggesting that inhibiting tau acetylation might have therapeutic potential in these disorders.
References
Min, S. W. et al. Critical role of acetylation in tau-mediated neurodegeneration and cognitive deficits. Nat. Med. http://dx.doi.org/10.1038/nm.3951 (2015)
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Lewis, S. Tackling TAUxicity. Nat Rev Neurosci 16, 646 (2015). https://doi.org/10.1038/nrn4046
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DOI: https://doi.org/10.1038/nrn4046