Lexical decision times to atypically presented words were, however, significantly delayed, showing that at later stages of processing, atypical presentation does create some type of interference.
One previous EEG study has already investigated the processing profile of atypically presented Japanese words [20].
The question though is, when should frequency affect the processing of the atypically presented hiragana stimuli?
and Typicality (F 1, 13) = 23.12, p<0.001), high frequency words eliciting faster decisions and atypically presented words slower.
In the left hemisphere, Typicality had a reliable main effect on M170 latency, atypically presented items eliciting later peaks than typically presented items (F 1,12) = 5.92, p<0.03).
In sum, in our second experiment, we took advantage of the millisecond temporal resolution of magnetoencephalography (MEG) to assess whether typically and atypically presented words would elicit an effect of frequency equally early.
However, in our data, M170 latencies did show a slight delay for atypically presented items, raising the possibility that the representations active at the M170 may not be script-invariant, even if the ones encoded at the M100 are.
As described above, our study differs from [20] in that in addition to script typicality, we varied form frequency (or familiarity), with the goal of assessing whether the atypically presented stimuli would nevertheless elicit an early effect of form familiarity, suggesting that they directly activate the abstract form representation of the word.
These mutations are often only partially disabling or present atypically, with patients lacking diagnostic features of the Mendelian disorders with which these genes are classically associated.
In ATXN2, polyQ expansions of ≥ 34, which are pure CAG repeat expansions, cause spinocerebellar ataxia type 2. However, similar length expansions that are interrupted with other codons, can present atypically with parkinsonism, suggesting that configuration of the repeat sequence plays an important role in disease manifestation in ATXN2 polyQ expansion diseases.
