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Abeta 38/40/42/43 - 218 103

A major component of neuritic plaques in Alzheimer's disease
Polyclonal rabbit purified antibody
Cat. No.: 218 103
Amount: 50 µg
Price: 370.00 €
Cat. No. 218 103 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: 1 : 1000 (ECL detection) (see remarks) gallery  
IP: not tested yet
ICC: not tested yet
IHC: 1 : 500 (see remarks) gallery  
IHC-P/FFPE: 1 : 500 (see remarks) gallery  
Immunogen Synthetic peptide corresponding to AA 1 to 16 from human Abeta (UniProt Id: P05067)
Reactivity Reacts with: human (P05067), rat (P08592), mouse (P12023).
Other species not tested yet.
Specificity Recognizes Abeta 38, 40, 42, 43.
Remarks

WB: Increased expression levels of Abeta required. Boil membrane after blotting for 3min.

IHC: Antigen retrieval with formic acid is required.

IHC-P: Antigen retrieval with formic acid is required.

Data sheet 218_103.pdf

References for Abeta 38/40/42/43 - 218 103

Phenotypic profile of alternative activation marker CD163 is different in Alzheimer's and Parkinson's disease.
Pey P, Pearce RK, Kalaitzakis ME, Griffin WS, Gentleman SM
Acta neuropathologica communications (2014) 2: 21. 218 103 IHC
Cat. No.: 218 103
Quantity: 50 µg
Price: 370.00 €
Phenotypic profile of alternative activation marker CD163 is different in Alzheimer's and Parkinson's disease.
Pey P, Pearce RK, Kalaitzakis ME, Griffin WS, Gentleman SM
Acta neuropathologica communications (2014) 2: 21. 218 103 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.