Pyroglutamate-modified amyloid-β (AβpE3) peptides are gaining considerable attention as potential key participants in the pathology of Alzheimer disease (AD) due to their abundance in AD brain, high aggregation propensity, stability, and cellular toxicity. Transgenic mice that produce high levels of AβpE3–42 show severe neuron loss. Recent in vitro and in vivo experiments have proven that the enzyme glutaminyl cyclase catalyzes the formation of AβpE3. In this minireview, we summarize the current knowledge on AβpE3, discussing its discovery, biochemical properties, molecular events determining formation, prevalence in the brains of AD patients, Alzheimer mouse models, and potential as a target for therapy and as a diagnostic marker.
Pyroglutamate Amyloid-β (Aβ): A Hatchet Man in Alzheimer Disease*
Sadim Jawhar,O. Wirths,T. Bayer
Published 2011 in Journal of Biological Chemistry
ABSTRACT
PUBLICATION RECORD
- Publication year
2011
- Venue
Journal of Biological Chemistry
- Publication date
2011-09-29
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
CITATION MAP
EXTRACTION MAP
CLAIMS
- No claims are published for this paper.
CONCEPTS
- No concepts are published for this paper.