IHC, Paraffin Sections (FFPE), Frozen Sections, Western Blot, ELISA
Reviews / Ratings
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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) 1-40/42/43 and additional C- and N-terminally modified fragments of Abeta as for instance Abeta pE3 and Abeta pE11. An additional Abeta variant, Abeta 38, is more soluble compared to other Abeta species and is not found in plaques of sporadic Alzheimer?s cases. However, it is detected in the blood-vessel walls of a subset of patients with severe cerebral amyloid angiopathy. It especially accumulates in brains of patients carrying mutations in the Abeta coding region.
Immunogen
Synthetic peptide (aa 1 - 16) of abeta peptides 38, 40, 42 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. / Antibody 9D5 Recognizes Oligomeric Pyroglutamate Amyloid-β in a Fraction of Amyloid-β Deposits in Alzheimer's Disease without Cross-Reactivity with other Protein Aggregates. Venkataramani V, Wirths O, Budka H, Hartig W, Kovacs GG & Bayer TA. Journal of Alzheimer's Disease 29: 361-71, 2012. / Overexpression of glutaminyl cyclase, the enzyme responsible for pyroglutamate abeta formation, induces behavioral deficits and glutaminyl cyclase knock-out rescues the behavioral phenotype in 5XFAD mice. Jawhar S, Wirths O, Schilling S, Graubner S, Demuth HU & Bayer TA. Journal of Biological Chemistry 286: 4454-60, 2010.