Increased glutaminyl cyclase expression in peripheral blood of Alzheimer's disease patients.

@article{Valenti2013IncreasedGC,
  title={Increased glutaminyl cyclase expression in peripheral blood of Alzheimer's disease patients.},
  author={Maria Teresa Valenti and Silvia Bolognin and Cristina Zanatta and Luca Donatelli and Giulio Innamorati and M. Pampanin and Gianluigi Zanusso and Paolo F. Zatta and Luca Dalle Carbonare},
  journal={Journal of Alzheimer's disease : JAD},
  year={2013},
  volume={34 1},
  pages={
          263-71
        }
}
N-truncated and N-modified forms of amyloid-β (Aβ) peptide are found in diffused and dense core plaques in Alzheimer's disease (AD) brain. Among them, the most abundant N-truncated peptide starts with pyroglutamyl at residue 3 (AβpE3). AβpE3 has increased aggregation potential and toxicity and its abundance has been reported to correlate with the severity of the clinical phenotype in AD patients. N-terminal glutamate conversion generating AβpE3 is catalyzed by glutaminyl cyclase. This enzyme… 
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Observations provide evidence for an involvement of QC in AD pathogenesis and cognitive decline by QC-catalyzed pGlu-Aβ formation.
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The properties and localization of two pyroglutamate-modified Aβ peptides, A βN3(pE) and AβN11( pE), in the brain are described and the role of glutaminyl cyclase (QC) in the formation of these peptides is addressed.
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  • Biology, Chemistry
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This review summarizes the patents/applications regarding QC inhibitors released from 2004 (first patent) to now and describes in terms of chemical structures, biochemical/pharmacological activities, and potential clinical applications.
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