Abstract:
:Anosmia affects the western world population, mostly the elderly, reaching to 5% in subjects over the age of 45 years and strongly lowering their quality of life. A smaller minority (about 0.01%) is born without a sense of smell, afflicted with congenital general anosmia (CGA). No causative genes for human CGA have been identified yet, except for some syndromic cases such as Kallman syndrome. In mice, however, deletion of any of the 3 main olfactory transduction components (guanidine triphosphate binding protein, adenylyl cyclase, and the cyclic adenosine monophosphate-gated channel) causes profound reduction of physiological responses to odorants. In an attempt to identify human CGA-related mutations, we performed whole-genome linkage analysis in affected families, but no significant linkage signals were observed, probably due to the small size of families analyzed. We further carried out direct mutation screening in the 3 main olfactory transduction genes in 64 unrelated anosmic individuals. No potentially causative mutations were identified, indicating that transduction gene variations underlie human CGA rarely and that mutations in other genes have to be identified. The screened genes were found to be under purifying selection, suggesting that they play a crucial functional role not only in olfaction but also potentially in additional pathways.
journal_name
Chem Sensesjournal_title
Chemical sensesauthors
Feldmesser E,Bercovich D,Avidan N,Halbertal S,Haim L,Gross-Isseroff R,Goshen S,Lancet Ddoi
10.1093/chemse/bjl032subject
Has Abstractpub_date
2007-01-01 00:00:00pages
21-30issue
1eissn
0379-864Xissn
1464-3553pii
bjl032journal_volume
32pub_type
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