beta Amyloid Polyclonal Antibody, Rockland™

Description

• Store vial at -20°C prior to opening
• Aliquot contents and freeze at -20°C or below for extended storage
• Avoid cycles of freezing and thawing
• Centrifuge product if not completely clear after standing at room temperature
• This product is stable for several weeks at 4°C as an undiluted liquid
• Dilute only prior to immediate use
• This affinity-purified antibody is directed against the amino terminal end of beta amyloid and is useful in determining its presence in various assays
• Polyclonal anti-beta amyloid detects human and mouse beta amyloid
• Cross reactivity with beta amyloid from other species is likely but has not been determined
• Amyloid beta peptide (Abeta/Beta-amyloid) is the major constituent of amyloid plaques in the brains of individuals afflicted with Alzheimer's disease
• Abeta peptide is 40-43 amino acids long and generated from the beta-amyloid precursor protein (beta APP) in a two-step process
• The first step involves cleavage of the extracellular, amino-terminal domain of beta APP
• Protein cleavage is performed by an aspartyl protease, beta-secretase (BACE) which is synthesized as a propeptide and must be modified to the mature and active form by the prohormone convertase, furin
• Beta APP cleavage by the mature form of BACE results in the cellular secretion of a segment of beta APP, and a membrane-bound remnant
• The remnant protein is processed by another protease, gamma-secretase
• Gamma-secretase cleaves an intra-membrane site in the carboxyl-terminal domain of beta APP, thus generating the amyloid beta peptide
• Gamma-secretase is believed to be a multi-subunit complex containing presenilin-1 and 2 as central components
• The transmembrane glycoprotein, nicastrin, is associated with presinilins and has been found to bind to the carboxyl-terminus of beta APP and helps to modulate the production of the amyloid beta peptide
• Abeta is an extracellular filamentous protein component of amyloid cores, neuritic plaques and is also found as a deposit in neurofibrillary tangles
• Alzheimer’s disease, the most common cause of senile dementia, is characterized by abnormal filamentous protein deposits in the brain
• Beta amyloid deposits are also detected in Lewy body dementia, Down’s syndrome, amyloidosis (Dutch type), cerebroarterial amyloidosis (cerebral amyloid angiopathy) and in the Guam Parkinson-Dementia complex.