Home|||||||Technical Support|

Abeta 38/40/42/43 - 218 113

A major component of neuritic plaques in Alzheimer's disease
Polyclonal rabbit purified antibody
Cat. No.: 218 113
Amount: 50 µg
Price: 370.00 €
Cat. No. 218 113 50 µg specific antibody, lyophilized. Affinity purified with the immunogen. Albumin was added for stabilization. For reconstitution add 50 µl H2O to get a 1mg/ml solution in PBS. Then aliquot and store at -20°C until use.
Applications WB: not tested yet
IP: not tested yet
ICC: not tested yet
IHC: 1 : 100 up to 1 : 500 (see remarks) gallery  
IHC-P/FFPE: 1 : 1000 (see remarks) gallery  
ELISA: not tested yet
Immunogen Synthetic peptide corresponding to AA 13 to 29 from human Abeta (UniProt Id: P05067)
Reactivity Reacts with: human (P05067), mouse (P12023), dog.
Other species not tested yet.
Specificity Recognizes Abeta 38, 40, 42, 43.
Remarks

IHC: Antigen retrieval with formic acid is required.

IHC-P: Antigen retrieval with formic acid increases sensitivity and reveals more plaques.

Data sheet 218_113.pdf

References for Abeta 38/40/42/43 - 218 113

Aβ38 in the brains of patients with sporadic and familial Alzheimer's disease and transgenic mouse models.
Reinert J, Martens H, Huettenrauch M, Kolbow T, Lannfelt L, Ingelsson M, Paetau A, Verkkoniemi-Ahola A, Bayer TA, Wirths O
Journal of Alzheimer's disease : JAD (2014) 394: 871-81. 218 113 WB; tested species: human
Neurovascular Specifications in the Alzheimer-Like Brain of Mice Affected by Focal Cerebral Ischemia: Implications for Future Therapies.
Michalski D, Hofmann S, Pitsch R, Grosche J, Härtig W
Journal of Alzheimer's disease : JAD (2017) 592: 655-674. 218 113 IHC; tested species: mouse
Detection and Quantification of β-Amyloid, Pyroglutamyl Aβ, and Tau in Aged Canines.
Schmidt F, Boltze J, Jäger C, Hofmann S, Willems N, Seeger J, Härtig W, Stolzing A
Journal of neuropathology and experimental neurology (2015) 749: 912-23. 218 113 IHC
Cat. No.: 218 113
Quantity: 50 µg
Price: 370.00 €
Aβ38 in the brains of patients with sporadic and familial Alzheimer's disease and transgenic mouse models.
Reinert J, Martens H, Huettenrauch M, Kolbow T, Lannfelt L, Ingelsson M, Paetau A, Verkkoniemi-Ahola A, Bayer TA, Wirths O
Journal of Alzheimer's disease : JAD (2014) 394: 871-81. 218 113 WB; tested species: human
Neurovascular Specifications in the Alzheimer-Like Brain of Mice Affected by Focal Cerebral Ischemia: Implications for Future Therapies.
Michalski D, Hofmann S, Pitsch R, Grosche J, Härtig W
Journal of Alzheimer's disease : JAD (2017) 592: 655-674. 218 113 IHC; tested species: mouse
Detection and Quantification of β-Amyloid, Pyroglutamyl Aβ, and Tau in Aged Canines.
Schmidt F, Boltze J, Jäger C, Hofmann S, Willems N, Seeger J, Härtig W, Stolzing A
Journal of neuropathology and experimental neurology (2015) 749: 912-23. 218 113 IHC
Background

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.
Cleavage of amyloid precursor protein APP by β- and γ- secretases results in the generation of the Aβ (βA4)peptide, whereas α-secretase cleaves within the Aβ sequence and prevents the formation of Abeta from APP.