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. Author manuscript; available in PMC: 2018 Jul 1.
Published in final edited form as: J Neurol Neurosurg Psychiatry. 2017 May 13;88(7):575–585. doi: 10.1136/jnnp-2016-315077

Table 2.

Mutation frequency, mode of transmission, age of onset and neurophysiological features (n=67 kindreds)

NEFL amino
acid change
Exon Domain Subdomain Kindreds,
n (%)
Familial
cases,
n
Individual
cases,
n
Confirmed
inheritance
patterns
De novo
mutation,
n (cases)
AOO,
range
(decade)
AOO ≤3 years,
n (cases)
Median
MNCV,
range
(m/s)
Ulnar
MNCV,
range
(m/s)
P8L 1 Head 2 (3) 2 SP 1 1 1 13–33 19
P8Q 1 Head 1 (1.5) 1 1 21 33
P8R 1 Head 7 (10.4) 27 3 AD, SP 1 1–3 23–41 30–49
T21Afs*83 1 Head 1 (1.5) 1
P22R 1 Head 1 (1.5) 5 AD 1–2 1 22–29 24–25
P22S 1 Head 7 (10.4) 71 1 AD 1–5 21–54 22–59
P22T 1 Head 2 (3) 5 AD 2–3 21–36 33–39
E90K 1 Head 2 (3) 2 SP 2 1 2 17–27 28
L94P 1 Rod Coil 1A 1 (1.5) 10 AD 1–2 35–38 29–40
N98S 1 Rod Coil 1A 10 (14.9) 4 8 AD, SP 4 1–2 11 18–35§ 23–33§
N98T 1 Rod Coil 1A 1 (1.5) 1 1 1 44
E140* 1 Rod Coil 1B 1 (1.5) 2 AR 1 14
A149V 1 Rod Coil 1B 1 (1.5) 1 4
E186* 1 Rod Coil 1B
E210* 1 Rod Coil 1B 1 (1.5) 4 AR 1 4 12–25 14–23
Y265C 1 Rod Coil 2A 1 (1.5) 7 AD
L268R 1 Rod Coil 2A 1 (1.5) 8 AD
L268P 1 Rod Coil 2A 2 (3) 17 AD 1–5 38–55 35–56
L311P 1 Rod Coil 2B 1 (1.5) 3 6 45–55 43–48
C322_N326del 1 Rod Coil 2B 1 (1.5) 11 AD 1 39–46 37–43
Q332P 1 Rod Coil 2B 3 (4.5) 21 1 AD 2–3 38–52
L333P 1 Rod Coil 2B 1 (1.5) 1
Q334P 1 Rod Coil 2B
L336P 1 Rod Coil 2B 1 (1.5) 1
I384F 2 Rod Coil 2B 1 (1.5) 22 AD 1–4 34–46 32–46
Y389C 2 Rod Coil 2B 1 (1.5) 9 AD 6 48–49 50–52
E396K 3 Rod Coil 2B 13 (19.4) 63 3 AD 1–6 5 29–63 25–58
R421* 3 Tail Subdomain A
F439I 3 Tail Subdomain A 1 (1.5) 1 3 45
P440L 3 Tail Subdomain A 2 (3) 3 1 AD 3
Total/range 67 (100) 293 27 8 1–6 25 12–63 14–59

Families or isolated cases with positive family history.

Based on cosegregation analysis.

§

Proximal nerve segments excluded.

AD, autosomal dominant; AOO, age of disease onset; AR, autosomal recessive; MNCV, motor nerve conduction velocities; SP, sporadic.

For two mutations (E186* and Q334P), there was no clinical data available.40 43 R421* has been reported in a family with an overlapping myopathic–neurogenic phenotype39 and also in association with CMT40 but no clinical details were available for the latter.

Of the remainder 27 mutations, 17 were private to a single kindred and 10 were observed in two or more kindreds. Twenty-four mutations were clustered in six regions of the NFL polypeptide (figure 4): the initial segment of the head domain (amino acid positions 8–22), the junction between the head and the rod domains (90–98), coil 2A (265–268), the mid portion of coil 2B (311–336), the end portion of coil 2B (384–396) and the tail subdomain A (421–440). Mutations in the head domain and the two ends of the rod domain accounted for 75% of kindreds and four common mutations within these regions (P8R, P22S, N98S and E396K) were observed in 55% of kindreds. Only three mutations (E140*, A149V and E210*) were located in coil 1B. No mutations were observed in linker regions of the rod domain or the tail subdomain B.