Polarimetric imaging for cancer diagnosis and staging

A medical imaging technique that relies on light polarization could become a fast and accurate optical method for detecting cancer and determining the stage of the disease

Evaluating β-amyloidosis progression in Alzheimer’s disease with Mueller polarimetry

We applied the wide-field Mueller imaging polarimetry for the screening of formalin-fixed paraffin-embedded samples of mouse brain tissue at different stages of brain β-amyloidosis in Alzheimer’s disease (AD). The accumulation of amyloid-beta (Aβ) deposits throughout the brain tissue is one of the key pathological hallmarks observed with the AD progression. We demonstrate that the presence of Aβ plaques influences the properties of backscattered polarized light, in particular, its degree of depolarization. By means of statistical analysis, we demonstrate that the high-order statistical moments of depolarization distributions, acquired with the multi-spectral Mueller imaging polarimetry, can be used as sensitive markers of the growing presence of Aβ plaques. The introduced label-free polarimetric approach has a potential to facilitate the current practice of the histopathology screening in terms of diagnosis accuracy, time and cost efficiency

The use of Stokes-Mueller polarimetry for assessment of amyloid-β progression in a mouse model of Alzheimer's disease

Alzheimer's disease, being a major societal burden, demands improvement of current techniques for its treatment and diagnostics. Currently only autopsy histology is able to provide the definite diagnosis for Alzheimer's disease. However, the procedure is rather time consuming and costly. In the current study, we utilized Stokes and Mueller polarimetry techniques to screen for amyloid-β (Aβ) deposits in formalin-fixed, paraffin-embedded mouse brain tissue at different stages of Alzheimer's disease. The study has shown that the presence of Aβ plaques influences the properties of scattered polarized light. The Poincaré sphere was used as a graphical tool for the visualization of the alterations of the Stokes vector, obtained with Stokes polarimetry, whereas statistical moments were used for the analysis of depolarization distributions that were acquired with Mueller polarimetry. We demonstrate the sensitivity of the last component of the Stokes vector, the degree of polarization and high-order statistical moments of depolarization to the structural alterations in brain tissue, which correspond to the disease progression. The described approach has a potential to improve the existing pathology screening methods and facilitates Aβ detection in AD research

The origins of polarimetric image contrast between healthy and cancerous human colon tissue

International audienceExperimentally measured spectral Mueller matrix images of ex vivo human colon tissue revealed the contrast enhancement between healthy and cancerous zones of colon specimen compared to unpolarized intensity images. Cancer development starts with abnormal changes which being not yet visible macroscopically may alter the polarization of reflected light. We have shown with experiments and modeling that light scattering by small (sub wavelength) scatterers and light absorption (mainly due to blood hemoglobin) are the key factors for observed polarimetric image contrast. These findings can pave the way for the alternative optical technique for the monitoring and early detection of cancer

Robustness of the wide-field imaging Mueller polarimetry for brain tissue differentiation and white matter fiber tract identification in a surgery-like environment: an ex vivo study.

During neurooncological surgery, the visual differentiation of healthy and diseased tissue is often challenging. Wide-field imaging Muller polarimetry (IMP) is a promising technique for tissue discrimination and in-plane brain fiber tracking in an interventional setup. However, the intraoperative implementation of IMP requires realizing imaging in the presence of remanent blood, and complex surface topography resulting from the use of an ultrasonic cavitation device. We report on the impact of both factors on the quality of polarimetric images of the surgical resection cavities reproduced in fresh animal cadaveric brains. The robustness of IMP is observed under adverse experimental conditions, suggesting a feasible translation of IMP for in vivo neurosurgical applications

Increased endocannabinoid levels reduce the development of precancerous lesions in the mouse colon

Colorectal cancer is an increasingly important cause of death in Western countries. Endocannabinoids inhibit colorectal carcinoma cell proliferation in vitro. In this paper, we investigated the involvement of endocannabinoids on the formation of aberrant crypt foci (ACF, earliest preneoplastic lesions) in the colon mouse in vivo. ACF were induced by azoxymethane (AOM); fatty acid amide hydrolase (FAAH) and cannabinoid receptor messenger ribonucleic acid (mRNA) levels were analyzed by the quantitative reverse transcription polymerase chain reaction (RT-PCR); endocannabinoid levels were measured by liquid chromatography–mass spectrometry; caspase-3 and caspase-9 expressions were measured by Western blot analysis. Colonic ACF formation after AOM administration was associated with increased levels of 2-arachidonoylglycerol (with no changes in FAAH and cannabinoid receptor mRNA levels) and reduction in cleaved caspase-3 and caspase-9 expression. The FAAH inhibitor N-arachidonoylserotonin increased colon endocannabinoid levels, reduced ACF formation, and partially normalized cleaved caspase-3 (but not caspase-9) expression. Notably, N-arachidonoylserotonin completely prevented the formation of ACF with four or more crypts, which have been show to be best correlated with final tumor incidence. The effect of N-arachidonoylserotonin on ACF formation was mimicked by the cannabinoid receptor agonist HU-210. No differences in ACF formation were observed between CB1 receptor-deficient and wild-type mice. It is concluded that pharmacological enhancement of endocannabinoid levels (through inhibition of endocannabinoid hydrolysis) reduces the development of precancerous lesions in the mouse colon. The protective effect appears to involve caspase-3 (but not caspase-9) activation

Garcinoic acid prevents β-amyloid (Aβ) deposition in the mouse brain

Garcinoic acid (GA or δ-T3-13'COOH), is a natural vitamin E metabolite that has preliminarily been identified as a modulator of nuclear receptors involved in β-amyloid (Aβ) metabolism and progression of Alzheimer's disease (AD). In this study, we investigated GA's effects on Aβ oligomer formation and deposition. Specifically, we compared them with those of other vitamin E analogs and the soy isoflavone genistein, a natural agonist of peroxisome proliferator-activated receptor γ (PPARγ) that has therapeutic potential for managing AD. GA significantly reduced Aβ aggregation and accumulation in mouse cortical astrocytes. Similarly to genistein, GA up-regulated PPARγ expression and apolipoprotein E (ApoE) efflux in these cells with an efficacy that was comparable with that of its metabolic precursor δ-tocotrienol and higher than those of α-tocopherol metabolites. Unlike for genistein and the other vitamin E compounds, the GA-induced restoration of ApoE efflux was not affected by pharmacological inhibition of PPARγ activity, and specific activation of pregnane X receptor (PXR) was observed together with ApoE and multidrug resistance protein 1 (MDR1) membrane transporter up-regulation in both the mouse astrocytes and brain tissue. These effects of GA were associated with reduced Aβ deposition in the brain of TgCRND8 mice, a transgenic AD model. In conclusion, GA holds potential for preventing Aβ oligomerization and deposition in the brain. The mechanistic aspects of GA's properties appear to be distinct from those of other vitamin E metabolites and of genistein