In the R6/2 mouse model of HD, genetic depletion of HDAC6 led to a significant increase in tubulin acetylation throughout the brain, but did not impact the onset and progression of various behavioral, physiological, molecular, and pathological HD-related phenotypes, nor did it affect the aggregate load or levels of soluble mutant exon 1 transprotein or the efficiency of BDNF transport from the cortex to the striatum, indicating that HDAC6 inhibition does not alter disease progression in R6/2 mice and should not be prioritized as a therapeutic target for HD [78]. Here, BDNF is linked to Huntington disease.