Dual Photonics Probing of Nano- to Submicron-Scale Structural Alterations in Human Brain Tissues or Cells and Chromatin or DNA with the Progression of Alzheimers Disease

TL;DR

This study introduces a dual photonics approach combining PWS and IPR techniques to detect nano- to submicron-scale structural alterations in brain tissues, cells, DNA, and chromatin associated with Alzheimer's progression.

Contribution

It presents a novel dual photonics method for early detection of Alzheimer's-related structural changes at nano to submicron scales in tissues and genetic material.

Findings

Significant increase in structural disorder at various stages of AD.

Structural disorder correlates with amyloid beta deposition and DNA damage.

Dual photonics techniques effectively differentiate AD progression stages.

Abstract

Understanding alterations in structural disorders in tissue or cells or building blocks, such as DNA or chromatin in the human brain, at the nano to submicron level provides us with efficient biomarkers for Alzheimers detection. Here, we report a dual photonics technique to detect nano- to submicron-scale alterations in brain tissues or cells and DNA or chromatin due to the early to late progression of Alzheimers disease in humans. Using a recently developed mesoscopic light transport technique, fine-focused nano-sensitive partial wave spectroscopy (PWS), we measure the degree of structural disorder in tissues. Furthermore, the chemical-specific inverse participation ratio technique (IPR) was used to measure the DNA or chromatin structural alterations. The results of the PWS and IPR experiments showed a significant increase in the degree of structural disorder at the nano to submicron scale at different stages of AD relative to their controls for both the tissue or cell and DNA cellular levels. The increase in the structural disorder in cells or tissues and DNA or chromatin in the nuclei can be attributed to higher mass density fluctuations in the tissue and DNA or chromatin damage in the nuclei caused by the rearrangements of macromolecules due to the deposition of the amyloid beta protein and damage in DNA or chromatin with the progress of AD.