Abstract
.Significance: Amyloid-beta () plaques are pathological protein deposits formed in the brain of Alzheimer’s disease (AD) patients upon disease progression. Further research is needed to elucidate the complex underlying mechanisms involved in their formation using label-free, tissue preserving, and volumetric techniques.Aim: The aim is to achieve a one-to-one correlation of optical coherence tomography (OCT) data to histological micrographs of brain tissue using 1060-nm swept source OCT.Approach: plaques were investigated in ex-vivo AD brain tissue using OCT with the capability of switching between two magnifications. For the exact correlation to histology, a 3D-printed tool was designed to generate samples with parallel flat surfaces. Large field-of-view (FoV) and sequentially high-resolution volumes at different locations were acquired. The large FoV served to align the OCT to histology images; the high-resolution images were used to visualize fine details.Results: The instrument and the presented method enabled an accurate correlation of histological micrographs with OCT data. plaques were identified as hyperscattering features in both FoV OCT modalities. The plaques identified in volumetric OCT data were in good agreement with immunohistochemically derived micrographs.Conclusion: OCT combined with the 3D-printed tool is a promising approach for label-free, nondestructive, volumetric, and fast tissue analysis.
Highlights
Alzheimer’s disease (AD) is the most common form of dementia worldwide
We present the investigation of A-β plaques in ex-vivo human brain tissue samples using a 1060-nm swept source optical coherence tomography (OCT) (SS-OCT) setup
A-β plaques were identified as highly scattering features within the gray matter in OCT images and as brownish accumulations in the immunohistochemically stained histology images; see Fig. 5
Summary
Alzheimer’s disease (AD) is the most common form of dementia worldwide. In 2019, 5.8 million people in the United States were suffering from AD. The numbers are increasing in our aging society, and there is still no cure available.[1] Our society is facing a considerable social and financial burden due to severe cognitive impairment of affected patients. They are dependent on care-giving.[1] On a cellular level, AD is characterized by the degeneration of neurons and the formation of intracellular neurofibrillary tangles composed of tau protein and extracellular plaques composed of amyloid-beta (A-β) protein.[2,3] The definite diagnosis of the disease can only be done postmortem by histologic analyses of different regions of the cerebral cortex. A-β plaques are in the range of 10 to 200 μm in diameter and have been investigated using light and fluorescence microscopy as well as Raman spectroscopy.[2,3,5,6,7,8] For these imaging techniques, processing steps such as sectioning and molecular labeling of the tissue are required
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