Literature DB >> 33144514

The genetic landscape of axonal neuropathies in the middle-aged and elderly: Focus on MME.

Jan Senderek1, Petra Lassuthova2, Dagmara Kabzińska2, Lisa Abreu2, Jonathan Baets2, Christian Beetz2, Geir J Braathen2, David Brenner2, Joline Dalton2, Lois Dankwa2, Tine Deconinck2, Peter De Jonghe2, Bianca Dräger2, Katja Eggermann2, Melina Ellis2, Carina Fischer2, Tanya Stojkovic2, David N Herrmann2, Rita Horvath2, Helle Høyer2, Stephan Iglseder2, Marina Kennerson2, Katharina Kinslechner2, Jennefer N Kohler2, Ingo Kurth2, Nigel G Laing2, Phillipa J Lamont2, Löscher Wolfgang N2, Albert Ludolph2, Wilson Marques2, Garth Nicholson2, Royston Ong2, Susanne Petri2, Gianina Ravenscroft2, Adriana Rebelo2, Giulia Ricci2, Sabine Rudnik-Schöneborn2, Anja Schirmacher2, Beate Schlotter-Weigel2, Ludger Schoels2, Rebecca Schüle2, Matthis Synofzik2, Bruno Francou2, Tim M Strom2, Johannes Wagner2, David Walk2, Julia Wanschitz2, Daniela Weinmann2, Jochen Weishaupt2, Manuela Wiessner2, Reinhard Windhager2, Peter Young2, Stephan Züchner2, Stefan Toegel2, Pavel Seeman2, Andrzej Kochański2, Michaela Auer-Grumbach1.   

Abstract

OBJECTIVE: To test the hypothesis that monogenic neuropathies such as Charcot-Marie-Tooth disease (CMT) contribute to frequent but often unexplained neuropathies in the elderly, we performed genetic analysis of 230 patients with unexplained axonal neuropathies and disease onset ≥35 years.
METHODS: We recruited patients, collected clinical data, and conducted whole-exome sequencing (WES; n = 126) and MME single-gene sequencing (n = 104). We further queried WES repositories for MME variants and measured blood levels of the MME-encoded protein neprilysin.
RESULTS: In the WES cohort, the overall detection rate for assumed disease-causing variants in genes for CMT or other conditions associated with neuropathies was 18.3% (familial cases 26.4%, apparently sporadic cases 12.3%). MME was most frequently involved and accounted for 34.8% of genetically solved cases. The relevance of MME for late-onset neuropathies was further supported by detection of a comparable proportion of cases in an independent patient sample, preponderance of MME variants among patients compared to population frequencies, retrieval of additional late-onset neuropathy patients with MME variants from WES repositories, and low neprilysin levels in patients' blood samples. Transmission of MME variants was often consistent with an incompletely penetrant autosomal-dominant trait and less frequently with autosomal-recessive inheritance.
CONCLUSIONS: A detectable fraction of unexplained late-onset axonal neuropathies is genetically determined, by variants in either CMT genes or genes involved in other conditions that affect the peripheral nerves and can mimic a CMT phenotype. MME variants can act as completely penetrant recessive alleles but also confer dominantly inherited susceptibility to axonal neuropathies in an aging population.
© 2020 American Academy of Neurology.

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Year:  2020        PMID: 33144514      PMCID: PMC7836667          DOI: 10.1212/WNL.0000000000011132

Source DB:  PubMed          Journal:  Neurology        ISSN: 0028-3878            Impact factor:   9.910


  49 in total

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