Archival ReportFear Processing and Social Networking in the Absence of a Functional Amygdala
Section snippets
Methods and Materials
Background information on Urbach-Wiethe disease and a detailed synopsis of all experimental procedures are provided in Supplement 1.
Molecular Genetics
The twins showed the same genotype in all sequenced regions. We found a novel homozygous missense mutation in exon 7 of ECM1, resulting in an exchange of tryptophan to arginine: c.709T>C; p.W237R (Figure S1 in Supplement 1). The alignment of proteins belonging to the ECM1 family confirmed that tryptophan 237 is highly conserved, thus underlining the potential pathogenic relevance of the p.W237R mutation (Figure S2 in Supplement 1).
Structural Imaging
The extracted volumes of interest did not significantly differ
Discussion
There is extensive evidence that patients with focal bilateral amygdala lesions are impaired in recognizing fear from faces (8, 9) and lack any subjective experience of fear ([6], but see [7]). However, substantial interindividual variability in the extent of these impairments (10) suggests the emergence of functional compensation to pathology in at least some amygdala-damaged patients. Here, we demonstrate a potential compensatory mechanism in one of monozygotic adult female twins with LP and
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Authors BB, YM, and DS contributed equally to this work.
Authors KMK and JSF contributed equally to this work.