Sequence 1287(Aducanumab)

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Sequence Aducanumab
Target beta-amyloid
Description BIIB-037 , Aducanumab

mab , source : human

Design Antibody
Chemistry Amino acids
Sequence Aducanumab heavy chain  : QVQLVESGGGVVQPGRSLRLSCAASGFAFSSYGMHWVRQAPGKGLEWVAVIWFDGTKKYYTDSVKGRFTISRDNSKNTLYLQMNTLRAEDTAVYYCARDRGIGARRGPYYMDVWGKGTTVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKRVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSREEMTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGxxxxxAducanumab light chain  : DIQMTQSPSSLSASVGDRVTITCRASQSISSYLNWYQQKPGKAPKLLIYAASSLQSGVPSRFSGSGSGTDFTLTISSLQPEDFATYYCQQSYSTPLTFGGGTKVEIKRTVAAPSVFIFPPSDEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTLSKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC
Application Alzheimer's disease
Name Aducanumab

References

Intrathecal Injections in Children With Spinal Muscular Atrophy: Nusinersen Clinical Trial Experience. Hache M, Swoboda KJ, Sethna N, Farrow-Gillespie A, Khandji A, Xia S, Bishop KM. J Child Neurol. 2016 Jun;31(7):899-906. PubMed:26823478

Comments

Background

Description. Alzheimer disease is the most common form of progressive dementia in the elderly. It is a neurodegenerative disorder characterized by the neuropathologic findings of intracellular neurofibrillary tangles (NFT) and extracellular amyloid plaques that accumulate in vulnerable brain regions (Sennvik et al., 2000). Terry and Davies (1980) pointed out that the 'presenile' form, with onset before age 65, is identical to the most common form of late-onset or 'senile' dementia, and suggested the term 'senile dementia of the Alzheimer type' (SDAT). Clinical Features. Alzheimer (1907) provided the first report of the disease (see HISTORY). Schottky (1932) described a familial form of presenile dementia in 4 generations. The diagnosis was confirmed at autopsy in a patient in the fourth generation. Lowenberg and Waggoner (1934) reported a family with unusually early onset of dementia in the father and 4 of 5 children. Postmortem findings in 1 case were consistent with dementia of the Alzheimer type. McMenemey et al. (1939) described 4 affected males in 2 generations with pathologic confirmation in one. Heston et al. (1966) described a family with 19 affected in 4 generations. Dementia was coupled with conspicuous parkinsonism and long tract signs.

Rice et al. (1980) and Ball (1980) reported a kindred in which members had clinical features of familial AD. Two patients had neuropathologic changes of spongiform encephalopathy of the Creutzfeldt-Jakob type (CJD; 123400) at autopsy, but the long clinical course was unusual for CJD. Corkin et al. (1983) found no difference in parental age of patients with AD compared to controls. Nee et al. (1983) reported an extensively affected kindred, with 51 affected persons in 8 generations. There was no increased incidence of Down syndrome (190685) or hematologic malignancy.

Heyman et al. (1983) found dementia in first-degree relatives of 17 (25%) of 68 probands with AD. These families also demonstrated an increase in the frequency of Down syndrome (3.6 per 1,000 as compared with an expected rate of 1.3 per 1,000). No excess of hematologic malignancy was found in relatives. In a study of the families of 188 Down syndrome children and 185 controls, Berr et al. (1989) found no evidence of an excess of dementia cases suggestive of AD in the families of patients with Down syndrome. In a large multicenter study of first-degree relatives of 118 AD probands and nondemented spouse controls, Silverman et al. (1994) found no association between familial AD and Down syndrome.

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