Clinical and pathological findings in familial amyloid polyneuropathy caused by a transthyretin E61K mutation
Author:
Funder
Kawasaki Medical School
KAKENHI
Publisher
Elsevier BV
Subject
Neurology (clinical),Neurology
Reference13 articles.
1. Genetics: clinical implications of TTR amyloidosis;Benson,2009
2. Genetic abnormalities and pathogenesis of familial amyloidotic polyneuropathy;Murakami;Pathol. Int.,1995
3. Familial amyloid polyneuropathy;Planté-Bordeneuve;Lancet Neurol.,2011
4. Schwann cells contribute to neurodegeneration in transthyretin amyloidosis;Murakami;J. Neurochem.,2015
5. Neurodegeneration in familial amyloid polyneuropathy: from pathology to molecular signaling;Sousa;Prog. Neurobiol.,2003
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1. Hereditary transthyretin amyloidosis: a myriad of factors that influence phenotypic variability;Journal of Neurology;2024-06-22
2. Clinical and biochemical characterization of hereditary transthyretin amyloidosis caused by E61K mutation;Frontiers in Molecular Neuroscience;2022-10-12
3. Magnetic resonance imaging of dorsal root ganglion in a pre-symptomatic subject with familial amyloid polyneuropathy transthyretin E61K;Journal of the Neurological Sciences;2022-09
4. Hereditary transthyretin amyloidosis in mainland China: a unicentric retrospective study;Annals of Clinical and Translational Neurology;2021-03-19
5. A low amyloidogenic E61K transthyretin mutation may cause familial amyloid polyneuropathy;Journal of Neurochemistry;2020-09-20
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