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J Neurol Neurosurg Psychiatry 2013 Nov; 84(11):e2
Authors: Graham Mackay, Helen Yull, James Ironside, Mark Head, Richard Knight
Southern General Hospital, Glasgow; National CJD research and surveillance unit, Edinburgh.
Sporadic CJD is a neurodegenerative illness first described in the 1920s. The condition is postulated to be spread by a process of direct protein to protein transmission. The prion hypothesis suggests that normal cellular proteins (PrPc) convert to an abnormal conformation (PrPSc), which forms a template for further protein misfolding. The variable phenotype of Sporadic CJD (sCJD) is largely felt to depend on a combination of the codon 129 genotype of the prion protein gene (MM, MV or VV) and the presence of the two major conformations of the protease-resistant prion protein (type 1 or type 2) in the brain. Cases were sub-classification on this basis into six discrete subtypes (MM1/MV1, VV1, MM2c, MM2t, MV2, VV2) with each characterised by a different clinico-pathological phenotype (Parchi et al, 1999). Recently a significant minority of patients have been found to have both protein types, challenging this classification system.
PMID: 24108956 [PubMed - as supplied by publisher]