Signs of excessive autophagy have been reported in patients with Alzheimer's disease (AD) but are uncommon in brains devoid of AD pathology (Nixon et al., 2005).
This impedes selection of a distinctive brain region devoid of tau ligand binding sites as reference tissue [7, 8].
Reference tissue models including MRTMO employ time-activity data in a brain region devoid of specific binding components as input functions.
Kinetic modelling with metabolite-corrected arterial plasma is considered the gold standard for quantification of [11C]PBR28 binding to the translocator protein (TSPO), since there is no brain region devoid of TSPO that can serve as reference.
(C) ChondroitinaseABC treatment was used to demonstrate that N-DMP1 was glycosylated; (D) Knock-in mouse strategies to change S89 to glycin, which eliminates N-DMP1 glycosylation; (E) Immunoblot showed that S89G-DMP1 brain was devoid of N-DMP1-PG.
Since there is no reference brain region devoid of TSPO [1], kinetic modelling with metabolite-corrected arterial plasma as input function is considered the gold standard for analysis of [11C]PBR28 binding, and the distribution volume (VT) is the commonly used outcome measure.
Our findings show that mild digestion with pronase E followed by detergent solubilisation and NaPTA precipitation produces a brain fraction devoid of PrPC that contains >70% of prion infectivity.
In addition to the local formation of pE-Aβ aggregates at sites of QC-immunoreactive somata, pE-Aβ peptides may be released in target areas of projection neurons and may form Aβ plaques in brain regions devoid of QC and/or APP expression.
