Bulletin of the American Physical Society
APS March Meeting 2022
Volume 67, Number 3
Monday–Friday, March 14–18, 2022; Chicago
Session Y06: Sub-cellular Structures: Droplets and Assemblies
8:00 AM–10:48 AM,
Friday, March 18, 2022
Room: McCormick Place W-178B
Sponsoring
Units:
DBIO DSOFT
Chair: Patrick McCall, Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG)
Abstract: Y06.00005 : Optical detection of structural alteration of brain tissues in progressive Alzheimer’s diseases using partial wave spectroscopy (PWS)
8:48 AM–9:00 AM
Presenter:
Pinki Chahal
(Mississippi State University)
Authors:
Pinki Chahal
(Mississippi State University)
Fatemah Alharthi
(Mississippi state university)
Pardeep shukla
(University of Tennessee)
Prakash Adhikari
(Mississippi state university)
Radhakrishna Rao
(University of Tennessee)
Mohammad Moshahid khan
(University of Tennessee)
Prabhakar Pradhan
(Mississippi State University)
Collaboration:
Pinki Chahal1, Fatemah Alherthi1, Pradeep Shukla2, Prakash Adhikari1, Radhakrishna Rao2, Mohammad Moshahid Khan2*, Prabhakar Pradhan1*
Alzheimer disease (AD) is the most common form of dementia, characterized pathologically by amyloid plaques and neurofibrillary tangles. One of the earliest overt signs of AD is a loss of cognitive function. It has been reported that AD affects the nanoscale structure of the brain cells which begins long before the cognitive symptoms appear. However, these alterations are undetectable in the initial stages with currently used bulk diagnostic techniques such as MRI and OCT. Thus, the elucidation of a neuroimaging method that can uniquely characterize these structural disorders at nanoscale is imperative for clinical diagnosis. Recently developed finer-focused partial wave spectroscopy (PWS) is a sensitive technique for probing nanoscale structural alterations in cells/tissues in terms of the average structural disorder strength. Results of PWS technique measurements of brain tissues from an animal model and human subjects show significant increase in the disorder strength with the progression of AD relative to their controls. The increased disorder strength can be explained by the higher mass density fluctuations caused by the rearrangements of macromolecules due to the deposition of the amyloid beta protein and damage in DNA with progress of AD. This structural alteration may be reflected in other clinical parameters for early detection of AD and possible treatment.
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