Shu G. Chen

TL;DR: The data indicate that the sporadic form of Creutzfeldt‐Jakob disease comprises a limited number of variants, and the methionine/valine polymorphism at codon 129 of the prion protein gene and two types of protease‐resistant prion proteins are the major determinants of these variants.

TL;DR: The data indicate that C1 is a major product of normal PrPc metabolism, generated by a cleavage that disrupts the neurotoxic and amyloidogenic region of PrP comprising residues 106-126, suggesting a role for C2 in prion diseases.

TL;DR: This review attempts to classify and characterise sporadic and familial Creutzfeldt-Jakob disease (CJD) as a function of these two disease determinants: PrP genotype and PrP(Sc) type.

TL;DR: It is demonstrated that wild-type LRRK2 expression caused mitochondrial fragmentation along with increased mitochondrial dynamin-like protein (DLP1), a fission protein, which was further exacerbated by expression of PD-associated mutants (R1441C or G2019S) in both SH-SY5Y and differentiated primary cortical neurons.

TL;DR: The results suggest that Cu interactions with Abeta could be responsible for causing the covalent cross-linking of Abeta in these structures.