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CMT 2B New Mutation

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CMT 2B New Mutation

ANN Seattle Poster Session Monday, April 27, 2009 3:30 PM

[iN2-1.001] A New RAB7 Mutation in a Large French Charcot-Marie-Tooth 2B Family

Emmanuelle Salort-Campana, Pouget, le Bernard, Marseille, France,

Michel R. Magistris, Armand Bottani, Geneva, Switzerland, is Brice, Paris

Cedex 13, France, Philippe Latour, Bron Cedex, France

OBJECTIVE:

To report a new pathogenic RAB7 mutation responsible of CMT2B.

BACKGROUND: Charcot-Marie-Tooth (CMT) type 2B is a dominant inherited axonal

neuropathy clinically characterised by marked distal weakness, prominent distal

sensory loss and high frequency of ulcers, infections and amputations of the

toes. Missense mutations of the small GTPase RAB7 have been reported as

causative of CMT2B.

DESIGN/METHODS: We describe a large French family with the typical clinical

features of CMT2B. Clinical, electrophysiological data were collected from 8

affected patients. DNA samples from 9 family members were tested for RAB7

mutation.

RESULTS: 8 family members were definitively affected upon clinical or

electrophysiological examination. Several affected members revealed pronounced

distal muscle weakness and wasting in the lower limbs and prominent distal

sensory loss witch were frequently complicated by mild foot ulcers, infections

and rare toe amputations. Electroneuromyography was consistent with a chronic

axonal neuropathy. Genetic analysis identified a new dominant mutation

consisting in a c.475G>A (p.Ala159 Thr) missense mutation in all affected

patients.

CONCLUSIONS/RELEVANCE: The clinical and electrophysiological data are quite

similar to the previous RAB7 reported families. RAB7 gene has to be tested

facing an apparently hereditary sensory neuropathy with only mild motor

involvement. The Ala159Thr is a new RAB7 missense mutation and only the fifth

reported mutation. It is located in the vicinity of 3 previous RAB7 reported

mutations, which affect amino-acids 157 to 161 and cluster in a highly conserved

region of the protein. This observation confirms the hypothesis that RAB7 is

responsible of CMT2B and highlight the functional importance of the region of

the protein clustered by the majority of mutations found to date.

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