Chronic NDE biomarkers known to increase for three to 12 months after TBI, including cellular prion protein (PrPc), synaptogyrin-3, P-T181-tau, P-S396-tau, Aβ42, and interleukin (IL)-6, were elevated significantly in subjects who had TBI and CI compared with controls with TBI but no CI.
A new article in Cell Reports by Gunther and colleagues (Cell Rep. 2019; 26:145-158) shows that an orally administered cellular prion protein antagonist can rescue synaptic and cognitive deficits in Alzheimer's mice overexpressing amyloid-β.
We focus primarily on the prion protein and propose a pathological mechanism in which the interaction between α-synuclein and prion protein leads to the formation of cofilin/actin rods, culminating in long-term potentiation impairment and cognitive dysfunction.
A patient with Creutzfeldt-Jakob disease (CJD) with prion protein (PrP) gene codon 180 mutation (CJD 180) experienced cognitive decline over the 1.5-year period before her death.
Our findings provide evidence that variability of the PRNP gene at codon 129 might contribute to accelerating the rate of earlier cognitive decline in DS subjects.
This case implies a worldwide distribution of FFI and also highlights the need for more aggressive clinical application of genomic analysis of the PrP gene and polysomnographic study in patients with insomnia and cognitive impairments.