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Segments with poli-Q expansions form antiparallel beta strands, and by hydrogen bonds the strands form a beta sheet structure, resulting in aggregation of these misfolded proteins as intranuclear inclusions, either as oligomers or larger aggregates [94 ]. The mutated ARs in the nucleus undergo partial proteolysis due to misfolding, resulting in the production of truncated forms of the poli-Q-expanded AR oligomers. The accumulation of mutant AR aggregates is regarded as protective [95. These aggregates are observed at light microscopy as inclusions in the nucleus and cytoplasm of affected motor and sensory neurons and those with no apparent signs of damage [92 ]. It has been found that the number of aggregates was not correlated with toxicity [88 ]. In addition, this same type of aggregate is seen in other tissues including scrotal skin and abdominal viscera [73 ]. There is clear evidence that mutated AR aggregation leads to transcriptional dysregulation in affected neurons [97 ].

 

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