Abstracts from the 20th International Symposium on Signal Transduction at the Blood-Brain Barriers

https://deepblue.lib.umich.edu/bitstream/2027.42/138963/1/12987_2017_Article_71.pd

Assessment of the Alzheimer progression with multiwavelength stokes polarimetry

Abstract Multiwavelength Stokes polarimetry imaging is used for screening fixed bulk mouse brain tissue blocks at different stages of Alzheimer’s disease, providing statistically significant difference sufficient for quantitative analysis of brain tissue

Screening of Alzheimer’s disease with multiwavelength stokes polarimetry in a mouse model

Abstract The minimum histological criterion for the diagnostics of Alzheimer’s disease (AD) in tissue is the presence of senile plaques and neurofibrillary tangles in specific brain locations. The routine procedure of morphological analysis implies time-consuming and laborious steps including sectioning and staining of formalin-fixed paraffin-embedded (FFPE) tissue. We developed a multispectral Stokes polarimetric imaging approach that allows characterization of FFPE brain tissue samples to discern the stages of AD progression without sectioning and staining the tissue. The Stokes polarimetry approach is highly sensitive to structural alterations of brain tissue, particularly to the changes in light scattering and birefringence. We present the results of the label-free non-destructive screening of FFPE mouse brain tissue and show several polarization metrics that demonstrate statistically significant differences for tissues at different stages of AD

3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitor Atorvastatin mediated effects depend on the activation status of target cells in PLP-EAE

Mix E, Ibrahim SM, Pahnke J, et al. 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitor Atorvastatin mediated effects depend on the activation status of target cells in PLP-EAE. Journal of Autoimmunity. 2006;27(4):251-265

Lethal recessive myelin toxicity of prion protein lacking its central domain

PrP(C)-deficient mice expressing prion protein variants with large amino-proximal deletions (termed PrP(ΔF)) suffer from neurodegeneration, which is rescued by full-length PrP(C). We now report that expression of PrP(ΔCD), a PrP variant lacking 40 central residues (94–134), induces a rapidly progressive, lethal phenotype with extensive central and peripheral myelin degeneration. This phenotype was rescued dose-dependently by coexpression of full-length PrP(C) or PrP(C) lacking all octarepeats. Expression of a PrP(C) variant lacking eight residues (114–121) was innocuous in the presence or absence of full-length PrP(C), yet enhanced the toxicity of PrP(ΔCD) and diminished that of PrP(ΔF). Therefore, deletion of the entire central domain generates a strong recessive-negative mutant of PrP(C), whereas removal of residues 114–121 creates a partial agonist with context-dependent action. These findings suggest that myelin integrity is maintained by a constitutively active neurotrophic protein complex involving PrP(C), whose effector domain encompasses residues 94–134