Role of Prion Protein Aggregation in Neurotoxicity

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Role of Prion Protein Aggregation in Neurotoxicity

In several neurodegenerative diseases, such as Parkinson, Alzheimer's, Huntington, and prion diseases, the deposition of aggregated misfolded proteins is believed to be responsible for the neurotoxicity that characterizes these diseases. Prion protein (PrP), the protein responsible of prion diseases, has been deeply studied for the peculiar feature of its misfolded oligomers that are able to pr...

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Prion Neurotoxicity 51 Prion Neurotoxicity: Insights from Prion Protein Mutants

The chemical nature of prions and the mechanism by which they propagate are now reasonably well understood. In contrast, much less is known about the identity of the toxic prion protein (PrP) species that are responsible for neuronal death, and the cellular pathways that these forms activate. In addition, the normal, physiological function of cellular PrP (PrPC) has remained mysterious, hamperi...

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Prion neurotoxicity: insights from prion protein mutants.

The chemical nature of prions and the mechanism by which they propagate are now reasonably well understood. In contrast, much less is known about the identity of the toxic prion protein (PrP) species that are responsible for neuronal death, and the cellular pathways that these forms activate. In addition, the normal, physiological function of cellular PrP (PrP(C)) has remained mysterious, hampe...

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The Role of Crowded Physiological Environments in Prion and Prion-like Protein Aggregation

Prion diseases and prion-like protein misfolding diseases are related to the accumulation of abnormal aggregates of the normal host proteins including prion proteins and Tau protein. These proteins possess self-templating and transmissible characteristics. The crowded physiological environments where the aggregation of these amyloidogenic proteins takes place can be imitated in vitro by the add...

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Prion protein dynamics before aggregation.

Prion diseases, like Alzheimer's disease and Parkinson disease, are rapidly progressive neurodegenerative disorders caused by misfolding followed by aggregation and accumulation of protein deposits in neuronal cells. Here we measure intramolecular polypeptide backbone reconfiguration as a way to understand the molecular basis of prion aggregation. Our hypothesis is that when reconfiguration is ...

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ژورنال

عنوان ژورنال: International Journal of Molecular Sciences

سال: 2012

ISSN: 1422-0067

DOI: 10.3390/ijms13078648