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Now Available from Sigma-RBI
Prod. Nos. A 1976 and A 2101
Tools for Alzheimer’s Disease Research
Alzheimer’s Disease (AD) is characterized by the deposition of extracellular senile
plaques whose major component is amyloid b peptide
(Ab), a Ab40 to Ab43 amino acid peptide
cleaved from amyloid precursor protein (APP) during apoptosis by b-secretase (e.g. BACE) and
by a putative g-secretase. Increased Ab
formation leads to the elevated extracellular
concentrations of the “longer forms” of Ab, Ab
42 or Ab43. These peptides have a greater
tendency to aggregate than Ab40 and, therefore, are considered to
be pathological.1 The
increased release of Ab42/Ab43 leads to
the abnormal deposition of Ab and the associated
neurotoxicity in the brains of affected individuals.2 Anti-Amyloid Peptide
b (Ab) antibodies
Ab42 and Ab43
(Prod. Nos. A 1976 and
A 2101, respectively) were generated in rabbit against
the synthetic, cleavage site-specific peptides, purified by epitope-specific affinity
chromatography and preabsorbed to remove any reactivity towards full-length
Ab40 and Ab42
or Ab43, where appropriate.
| Species reactivity |
Detects human, mouse and rat Ab42
and Ab43 |
| Formulation |
Solution in phosphate buffer, pH 7.4 |
| Applications |
Dot Blot: 0.05 to 1.0 µg/ml
ELISA: mice brain extracts, human kidney 293 cells3,4 1:200 dilution
Immunohistochemistry: mice brain extracts5
Immunoprecipitation: cerebral cortex extracts from AD patients6 |
| Storage |
Store at -70 °C. For extended storage, upon
initial thawing, freeze in working aliquots. Do not store in frost-free freezers.
|
| Size |
25 µg |
References:
- Sambamurti, K., et al., Advances in the cellular and molecular biology of the
b-amyloid protein in Alzheimer's disease. Neuromolecular Med.,
1, 1-31 (2002).
- Lorenzo, A., et al., Amyloid b interacts with the amyloid precursor protein:
a potential toxic mechanism in Alzheimer's disease. Nat. Neurosci., 3,
460-464 (2000).
- Vassar, R., et al., b-secretase cleavage of Alzheimer's amyloid precursor
protein by the transmembrane aspartic protease BACE. Science,
286, 735-741 (1999).
- Savage, M. J., et al., Turnover of amyloid b-protein in mouse brain and acute
reduction of its level by phorbol ester. J. Neurosci., 18, 1743-1752 (1998).
- Borchelt, D.R., et al., Accelerated amyloid deposition in the brains of transgenic mice coexpressing
mutant presenilin 1 and amyloid precursor proteins. Neuron, 19, 939-945 (1997).
- Russo, C., et al., Opposite roles of apolipoprotein E in normal brains and in Alzheimer's
disease. Proc. Natl. Acad. Sci. USA, 95, 15598-15602 (1998).
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