β Amyloid (Aβ) Antibody (Rabbit mAb) [B1A10] Datasheet

Biological Description

Specificity	β Amyloid (Aβ) Antibody (Rabbit mAb) [B1A10] detects endogenous levels of total β Amyloid (Aβ) protein.
Background	β-Amyloid (Aβ), the amyloid beta-peptide, is the peptide that deposits in plaques in the brain in Alzheimer’s disease (AD). According to the amyloid hypothesis, accumulation of Aβ in the brain is the primary influence driving AD pathogenesis. The rest of the disease process, including formation of neurofibrillary tangles that contain tau protein, follows from an imbalance between Aβ production and Aβ clearance. Aβ aggregates through a series of intermediates. Small, soluble oligomers form early in the aggregation process and can cause synaptic dysfunction. Aβ oligomers adversely affect synaptic structure and plasticity. Large insoluble deposits, such as plaques, may serve as reservoirs of these bioactive oligomers. Distinct protein aggregates are found in Alzheimer’s, Parkinson’s, Huntington’s and prion diseases, and a broadly similar process of neuronal dysfunction arises from diffusible oligomers of misfolded proteins in these other diseases. Aβ is therefore both a deposited peptide in plaques and a soluble oligomeric species that disturbs synapses, and it is a central target in studies of AD pathogenesis and therapy.

Specificity

β Amyloid (Aβ) Antibody (Rabbit mAb) [B1A10] detects endogenous levels of total β Amyloid (Aβ) protein.

Background

β-Amyloid (Aβ), the amyloid beta-peptide, is the peptide that deposits in plaques in the brain in Alzheimer’s disease (AD). According to the amyloid hypothesis, accumulation of Aβ in the brain is the primary influence driving AD pathogenesis. The rest of the disease process, including formation of neurofibrillary tangles that contain tau protein, follows from an imbalance between Aβ production and Aβ clearance. Aβ aggregates through a series of intermediates. Small, soluble oligomers form early in the aggregation process and can cause synaptic dysfunction. Aβ oligomers adversely affect synaptic structure and plasticity. Large insoluble deposits, such as plaques, may serve as reservoirs of these bioactive oligomers. Distinct protein aggregates are found in Alzheimer’s, Parkinson’s, Huntington’s and prion diseases, and a broadly similar process of neuronal dysfunction arises from diffusible oligomers of misfolded proteins in these other diseases. Aβ is therefore both a deposited peptide in plaques and a soluble oligomeric species that disturbs synapses, and it is a central target in studies of AD pathogenesis and therapy.

Usage Information

Application

WB, IP, IF

Dilution

WB	IP	IF
1:1000	1:50	1:800-1:1600

Reactivity

Human

Source

Rabbit Monoclonal Antibody

MW

Storage Buffer

PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage
(from the date of receipt)

-20°C (avoid freeze-thaw cycles), 2 years

References

https://pubmed.ncbi.nlm.nih.gov/12130773/
https://pubmed.ncbi.nlm.nih.gov/17245412/

β Amyloid (Aβ) Antibody (Rabbit mAb) [B1A10]

Biological Description

Usage Information

References

Application Data