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Fig. 2 | Orphanet Journal of Rare Diseases

Fig. 2

From: The P42 peptide and Peptide-based therapies for Huntington’s disease

Fig. 2

Model of action of P42. A- In pathologic conditions, cleavage of mutant polyQHtt is increased, leading to short N-terminal fragments mostly lacking P42. N17 domains self interact, bringing together polyQHtt proteins (nucleation step). Oligomers will further form parallel ß sheets, thereby enhancing the aggregation process [64]. B- Our model is that exogenous addition of P42 allows a protective effect of polyQHtt-induced defects by directly interacting with the N17 domain of the N-terminal part of polyQHtt, therefore preventing nucleation, and consequently oligomerisation and aggregation processes.

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