PDF DatasheetAntibody (Suitable for clinical applications)
| Specification | Recommendation |
|---|---|
| Recommended Dilution (Conc) | 1:50-1:100 |
| Pretreatment | Citrate Buffer pH 6.0 |
| Incubation Parameters | 30 min at RoomTemperature |
Prior to use, inspect vial for the presence of any precipitate or other unusual physical properties. These can indicate that the antibody has degraded and is no longer suitable for patient samples. Please run positive and negative controls simultaneously with all patient samples to account and control for errors in laboratory procedure. Use of methods or materials not recommended by enQuire Bio including change to dilution range and detection system should be routinely validated by the user.
beta-Amyloid Protein Information for Pathologists
Summary:
Amyloid beta (A4) precursor protein (APP) is part of the type 1 transmembrane protein family. The APP gene is located on chromosome 21 and encodes for a cell surface receptor and transmembrane precursor protein. There are three homologs of APP: APP, APLP1 and APLP2 (Mol Neurodegener 2011;6:27). Cleavage of APP sequentially by beta secretase (rate limiting step) and gamma secretase produces beta amyloid (amyloid beta, A4, Abeta) peptides of 40 – 43 amino acids, as well as other peptides that have transcriptional, antimicrobial, or antifungal activities (Curr Opin Neurol 2000;13:377). The beta amyloid sequence is unique to APP and is not present in APLP1 or APLP2.
Notable Clinical Features:
Alzheimer disease: progressive memory loss and cognitive impairment, mood and personality changes, depression, anxiety in part due to the accumulation of beta amyloid deposits in the brain. Cerebral amyloid angiopathy: dementia, intracranial hemorrhage due to beta amyloid deposits in the vasculature. Diagnosis Beta amyloid can be detected using Congo red staining, immunohistochemical staining or PET imaging. Alzheimer disease: the presence of beta amyloid plaques and neurofibrillary tangles is essential for the diagnosis of Alzheimer disease (Alzheimer Dementia 2012;8:1) but is not pathognomonic for the disease beta amyloid plaques may be seen in normal aging and neurofibrillary tangles can be present in other neurodegenerative disorders.
| beta-Amyloid Protein General Information | |
|---|---|
| Alternate Names | |
| Molecular Weight | |
| 86.9 kDa | |
| Chromosomal Location | |
| q21.3 [chr: 21] [chr_start: 25880550] [chr_end: 26171128] [strand: -1] | |
| Curated Database and Bioinformatic Data | |
| Gene Symbol | APP |
| Entrez Gene ID | 351 |
| RefSeq Protein Accession(s) | NP_001191230; NP_001191231; NP_001129602; NP_000475; NP_001191232; NP_958817; NP_958816; NP_001129488; NP_001129601; NP_001129603 |
| RefSeq mRNA Accession(s) | NM_001204302; NM_001204303; XM_024452075; NM_001136016; NM_001136129; NM_001136130; NM_000484; NM_001204301; NM_201414; NM_001136131; NM_201413; |
| RefSeq Genomic Accession(s) | NG_007376; NC_000021 |
| UniProt ID(s) | P05067 |
| PharmGKB ID(s) | PA24910 |
| KEGG Gene ID(s) | hsa:351 |
| Associated Diseases (KEGG IDs) | Alzheimer disease 1 (AD1) [MIM:104300]: A familial early-onset form of Alzheimer disease. It can be associated with cerebral amyloid angiopathy. Alzheimer disease is a neurodegenerative disorder characterized by progressive dementia, loss of cognitive abilities, and deposition of fibrillar amyloid proteins as intraneuronal neurofibrillary tangles, extracellular amyloid plaques and vascular amyloid deposits. The major constituents of these plaques are neurotoxic amyloid-beta protein 40 and amyloid-beta protein 42, that are produced by the proteolysis of the transmembrane APP protein. The cytotoxic C-terminal fragments (CTFs) and the caspase-cleaved products, such as C31, are also implicated in neuronal death. {ECO:0000269|PubMed:10097173, ECO:0000269|PubMed:10631141, ECO:0000269|PubMed:10656250, ECO:0000269|PubMed:10665499, ECO:0000269|PubMed:10677483, ECO:0000269|PubMed:10867787, ECO:0000269|PubMed:11063718, ECO:0000269|PubMed:11311152, ECO:0000269|PubMed:11528419, ECO:0000269|PubMed:12034808, ECO:0000269|PubMed:1302033, ECO:0000269|PubMed:1303239, ECO:0000269|PubMed:1303275, ECO:0000269|PubMed:1415269, ECO:0000269|PubMed:1465129, ECO:0000269|PubMed:15201367, ECO:0000269|PubMed:15365148, ECO:0000269|PubMed:15668448, ECO:0000269|PubMed:1671712, ECO:0000269|PubMed:1678058, ECO:0000269|PubMed:1908231, ECO:0000269|PubMed:1925564, ECO:0000269|PubMed:1944558, ECO:0000269|PubMed:8267572, ECO:0000269|PubMed:8290042, ECO:0000269|PubMed:8476439, ECO:0000269|PubMed:8577393, ECO:0000269|PubMed:8886002, ECO:0000269|PubMed:9328472, ECO:0000269|PubMed:9754958}. The disease is caused by mutations affecting the gene represented in this entry.; Cerebral amyloid angiopathy, APP-related (CAA-APP) [MIM:605714]: A hereditary localized amyloidosis due to amyloid-beta A4 peptide(s) deposition in the cerebral vessels. The principal clinical characteristics are recurrent cerebral and cerebellar hemorrhages, recurrent strokes, cerebral ischemia, cerebral infarction, and progressive mental deterioration. Patients develop cerebral hemorrhage because of the severe cerebral amyloid angiopathy. Parenchymal amyloid deposits are rare and largely in the form of pre-amyloid lesions or diffuse plaque-like structures. They are Congo red negative and lack the dense amyloid cores commonly present in Alzheimer disease. Some affected individuals manifest progressive aphasic dementia, leukoencephalopathy, and occipital calcifications. {ECO:0000269|PubMed:11409420, ECO:0000269|PubMed:12654973, ECO:0000269|PubMed:16178030, ECO:0000269|PubMed:20697050, ECO:0000269|PubMed:2111584}. The disease is caused by mutations affecting the gene represented in this entry. |
| General Description of beta-Amyloid Protein . | |
| This antibody reacts with beta-amyloid protein. This antibody stains amyloid plaques within the cortex, and amyloid deposits in blood vessels. beta-amyloid deposits are also detected in Lewy body dementia, Down syndrome, amyloidosis and in Gram-Parkinson dementia complex. The presence of a large number of neuritic plaques (senile) and neurofibrillary tangles in the cerebral cortex is used as a pathological marker for a disease state and presents the major criterion for the diagnosis of Alzheimer’s disease at autopsy. | |
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