Literature DB >> 1685700

Vitreous involvement in familial amyloidotic neuropathy: a genealogical and genetic study.

O Sandgren1, U Drugge, G Holmgren, A Sousa.   

Abstract

Extended genealogical studies stretching back to the 17th century were performed concerning the heredity patterns of vitreous involvement in Swedish patients with familial amyloidotic polyneuropathy (FAP). FAP is an autosomal dominant inherited disorder, characterized by extracellular deposition of amyloid and a clinical syndrome of peripheral and autonomic neuropathy. In addition, some patients show typical vitreous opacities. All patients had their origin in a restricted geographical area. Some main patterns arose from this study: 1) Patients who had vitreous opacities as the first symptom of FAP seem to form a separate group, with a distinct age of onset distribution; 2) The familial occurrence of vitreous opacities raises the possibility that other familial factors modify the expression of the FAP gene; 3) The mean age of onset for vitreous opacities is lower for homozygous than for heterozygous patients.

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Year:  1991        PMID: 1685700     DOI: 10.1111/j.1399-0004.1991.tb03117.x

Source DB:  PubMed          Journal:  Clin Genet        ISSN: 0009-9163            Impact factor:   4.438


  7 in total

1.  Ophthalmic manifestations in a Chinese family with familial amyloid polyneuropathy due to a TTR Gly83Arg mutation.

Authors:  T Liu; B Zhang; X Jin; W Wang; J Lee; J Li; H Yuan; X Cheng
Journal:  Eye (Lond)       Date:  2013-10-11       Impact factor: 3.775

2.  Age-dependent cognitive dysfunction in untreated hereditary transthyretin amyloidosis.

Authors:  Ana Martins da Silva; Sara Cavaco; Joana Fernandes; Raquel Samões; Cristina Alves; Márcio Cardoso; Jeffery W Kelly; Cecília Monteiro; Teresa Coelho
Journal:  J Neurol       Date:  2017-12-05       Impact factor: 4.849

Review 3.  Natural history and therapy of TTR-cardiac amyloidosis: emerging disease-modifying therapies from organ transplantation to stabilizer and silencer drugs.

Authors:  Adam Castaño; Brian M Drachman; Daniel Judge; Mathew S Maurer
Journal:  Heart Fail Rev       Date:  2015-03       Impact factor: 4.214

Review 4.  The genetic contribution to the phenotype.

Authors:  U Wolf
Journal:  Hum Genet       Date:  1995-02       Impact factor: 4.132

5.  Quantitative sensation and autonomic test abnormalities in transthyretin amyloidosis polyneuropathy.

Authors:  Dong Hwee Kim; Steven R Zeldenrust; Phillip A Low; Peter J Dyck
Journal:  Muscle Nerve       Date:  2009-09       Impact factor: 3.217

6.  Hereditary myopathy with lactic acidosis, succinate dehydrogenase and aconitase deficiency in northern Sweden: a genealogical study.

Authors:  U Drugge; M Holmberg; G Holmgren; B G Almay; H Linderholm
Journal:  J Med Genet       Date:  1995-05       Impact factor: 6.318

7.  Modifications of transthyretin in amyloid fibrils: analysis of amyloid from homozygous and heterozygous individuals with the Met30 mutation.

Authors:  C Thylén; J Wahlqvist; E Haettner; O Sandgren; G Holmgren; E Lundgren
Journal:  EMBO J       Date:  1993-02       Impact factor: 11.598

  7 in total

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