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Description
Amyloid deposits, also called plaques, of Alzheimer's patients consist of several protein components like the amyloid beta-peptides (Abeta, Aβ) 1-40/42 and additional C- and N-terminally truncated and modified fragments. Very abundant are the isoaspartate (isoAsp)-Abeta and pyroglutamyl (pGlu)-Abeta peptides. The latter are formed by cyclization of the N-terminal glutamate at position 3 or 11 catalyzed by glutaminyl cyclase (QC) resulting in very amyloidogenic and neurotoxic variants of Abeta; Abeta-pE3 and Abeta pE11. In contrast to extracellular plaques that do not perfectly correlate with Alzheimer?s disease intraneuronal Abeta accumulation and vascular Abeta deposits have gained more and more evidence to be among the crucial factors responsible for progressive neuron loss.
Immunogen
Synthetic peptide pyr-EFRHD coupled to key-hole limpet hemocyanin via an added C-terminal cysteine residue.
Oligomeric Pyroglutamate Amyloid-β is Present in Microglia and a Subfraction of Vessels in Patients with Alzheimer's Disease: Implications for Immunotherapy. Wirths O, Hillmann A, Pradier L, Hartig W & Bayer TA. Journal of Alzheimer's Disease, Mar 12 [Epub ahead of print], 2013. / Selective hippocampal neurodegeneration in transgenic mice expressing small amounts of truncated Aβ is induced by pyroglutamate-Aβ formation. Alexandru A, Jagla W, Graubner S, Becker A, Bauscher C, Kohlmann S, Sedlmeier R, Raber KA, Cynis H, Ronicke R, Reymann KG, Petrasch-Parwez E, Hartlage-Rubsamen M, Waniek A, Rossner S, Schilling S, Osmand AP, Demuth HU & von Horsten S. Journal of Neuroscience 31: 12790-801, 2011. / Glutaminyl cyclase contributes to the formation of focal and diffuse pyroglutamate (pGlu)-Aβ deposits in hippocampus via distinct cellular mechanisms. Hartlage-Rubsamen M, Morawski M, Waniek A, Jager C, Zeitschel U, Koch B, Cynis H, Schilling S, Schliebs R, Demuth HU & Ro ner S. Acta Neuropathologica 121: 705-19, 2011. / Motor deficits, neuron loss, and reduced anxiety coinciding with axonal degeneration and intraneuronal Abeta aggregation in the 5XFAD mouse model of Alzheimer's disease. Jawhar S, Trawicka A, Jenneckens C, Bayer TA & Wirths O. Neurobiology of Aging, Jul 8 [Epub ahead of print] 2010. / Concomitant detection of beta-amyloid peptides with N-terminal truncation and different C-terminal endings in cortical plaques from cases with Alzheimer's disease, senile monkeys and triple transgenic mice. Hartig W, Goldhammer S, Bauer U, Wegner F, Wirths O, Bayer TA & Grosche J. Journal of Chemical Neuroanatomy 40: 82-92 Clone 2-48, 2010. / Pyroglutamate Abeta pathology in APP/PS1KI mice, sporadic and familial Alzheimer's disease cases. Wirths O, Bethge T, Marcello A, Harmeier A, Jawhar S, Lucassen PJ, Multhaup G, Brody DL, Esparza T, Ingelsson M, Kalimo H, Lannfelt L & Bayer TA. Journal of Neural Transmission 117: 85-96. Clone 2-48, 2010.