Abstract:
:Mutations in APP are associated with familial early-onset Alzheimer disease (FAD). Examination of the genomic sequence in one patient with FAD revealed a change located in the axon 17 of the APP gene at position 275329G>A (GenBank accession number: D87675; GI: 2429080); cDNA sequence 2137G>A (GenBank accession number: X06989; GI: 28720). This corresponds to the mutation A713T in APP. AD stage VI of neurofibrillary degeneration and stage C of Abeta-amyloid burden was found at the post-mortem neuropathological examination. Previous studies have suggested that the mutation A713T in APP is a silent mutation or polymorphism. However, we have not found this change in APP in a control population analyzed by the amplification-refractory mutation system (ARMS). It is concluded that A713T in APP is implicated in the pathogenesis of AD. Since the immunohistochemical study indicates that A713T mutation is not likely to relate with Abeta-amyloid processing, the causative role of this rare mutation remains to be warranted.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Armstrong J,Boada M,Rey MJ,Vidal N,Ferrer Idoi
10.1016/j.neulet.2004.08.026keywords:
subject
Has Abstractpub_date
2004-11-11 00:00:00pages
241-3issue
2-3eissn
0304-3940issn
1872-7972pii
S0304-3940(04)01023-7journal_volume
370pub_type
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