This paper aims to study four general hallmarks of neurodegeneration and the correlations between them, with emphasis on the huntingtin (htt) interactions contributing to their prevention or promotion in its wild-type and mutated forms. Most of the neurodegenerative diseases share same or similar cell dysfunctions and huntingtin seems to associate in an polyglutamine-length dependent manner with components of the mechanisms that can go impaired. Therefore, the protein is proposed as contributing factor to the development of selective neurodegeneration.
Keywords: Degradation pathways; Huntingtin; Mitochondria; Neurodegeneration; PolyQ tract; Protein aggregation; Transcription.