Optical Taxonomic Signal and the Diagnosis of Alzheimer's Disease
Goal: We previously demonstrated that near-infrared spectroscopy in vivo presents spectral features at 895 and 861 nm that accurately classify Alzheimer's disease, mild cognitive impairment, and age-matched control subjects. Our purpose here is to associate the 895 nm signal with <inline-for...
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Published in | IEEE open journal of engineering in medicine and biology Vol. 6; pp. 107 - 112 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
United States
IEEE
01.01.2025
The Institute of Electrical and Electronics Engineers, Inc. (IEEE) |
Subjects | |
Online Access | Get full text |
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Summary: | Goal: We previously demonstrated that near-infrared spectroscopy in vivo presents spectral features at 895 and 861 nm that accurately classify Alzheimer's disease, mild cognitive impairment, and age-matched control subjects. Our purpose here is to associate the 895 nm signal with <inline-formula><tex-math notation="LaTeX">\beta</tex-math></inline-formula>-amyloid. Methods: We applied our feature selection technique to subjects with and without leptomeningeal amyloid. We developed a novel concept, optical taxonomic signal, to determine the dependence of signal on source-detector distance. Results: Features at 891 and 768 nm discriminate between subjects with and without leptomeningeal <inline-formula><tex-math notation="LaTeX">\beta</tex-math></inline-formula>-amyloid. The variation of optical taxonomic signal with source-detector distance indicates that both signals come from the leptomeninges and not cerebral cortex. The two features are highly correlated and likely result from the same cellular material. Conclusions: The discovery of an 891 nm feature that clearly depends upon the presence of <inline-formula><tex-math notation="LaTeX">\beta</tex-math></inline-formula>-amyloid supports our hypothesis that the 895 nm feature previously discovered also reports <inline-formula><tex-math notation="LaTeX">\beta</tex-math></inline-formula>-amyloid. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
ISSN: | 2644-1276 2644-1276 |
DOI: | 10.1109/OJEMB.2024.3477449 |