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Albayram et al., 2011)

The etiology of HD is primarily attributed to the huntingtin protein (HTT) gene contains an abnormal number of CAG repeats, leading to the amplification of trinucleotide repeat sequences (TNR), specifically the CAG codon, resulting in the synthesis of an abnormal protein with an expanded polyglutamine (polyQ) tract (210, 211)

Similarly, ICV pretreatment or peripheral post-treatment with the DEETGE-Cal-Tat peptide was also able to decrease Keap1-Nrf2 interaction in the rat hippocampal CA1 region after global cerebral ischemia (GCI) and, as a consequence, to induce Nrf2 target genes and a powerful neuroprotection of hippocampal-dependent cognitive function after GCI [302]

DISCLOSURES: The authors declare no conflicts of interest relevant to the content of this article