A role of mitochondrial complex II defects in genetic models of Huntington's disease expressing N-terminal fragments of mutant huntingtin.

Hum Mol Genet · 2013 · PMC3766181 · PMID 23720495

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closest p · 0.6× alpha

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highly significantP < 0.03actually significant

Analysis showed that the loss produced by Htt171-82Q was highly significant (two-way ANOVA; Htt171-82Q effect, F = 4.82, P < 0.03; Antero-posterior levels, F = 9.12, P < 0.003, and post hoc Bonferroni/Dunn test, P < 0.0017), although of minimal amplitude (∼10%), since the volume of infection was small compared with the entire striatum (Fig. 4 ).

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showed a trendno p-value reported

The expression of the Fp subunit showed a trend to decrease that did not reach significance (Fig. 6 ; Ip/actin ratio: lenti-Htt171-18Q, n = 6, 2.091 ± 0.252; lenti-Htt171-82Q, n = 6, 1.685 ± 0.304; unpaired Student's t -test, P < 0.02).

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