Acetylation unleashes protein demons of dementia

Mark P. Mattson

Research output: Contribution to journalArticlepeer-review

Abstract

Aberrant posttranslational modifications of proteins can impair synaptic plasticity and may render neurons vulnerable to degeneration during aging. In this issue of Neuron, Min et al. show that acetylation of the amino acid lysine in the microtubule-associated protein tau prevents its ubiquitin-mediated degradation, resulting in "tau tangles" similar to those of dementias. Other recent studies suggest that lysine hyperacetylation contributes to the accumulation of amyloid β-peptide in Alzheimer's disease and to impaired cognitive function resulting from a trophic factor deficit.

Original languageEnglish (US)
Pages (from-to)900-902
Number of pages3
JournalNeuron
Volume67
Issue number6
DOIs
StatePublished - Sep 2010
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)

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