Copper and zinc isotopic excursions in the human brain affected by Alzheimer's disease
Introduction Alzheimer's disease (AD) is neuropathologically marked by amyloid beta (Aβ) plaques and neurofibrillary tangles. Little is known about isotopic compositions of human AD brains. Here we study this in comparison with control subjects for copper and zinc. Methods We use mass‐spectrome...
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Published in | Alzheimer's & dementia : diagnosis, assessment & disease monitoring Vol. 12; no. 1; pp. e12112 - n/a |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
John Wiley & Sons, Inc
2020
Wiley John Wiley and Sons Inc |
Subjects | |
Online Access | Get full text |
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Summary: | Introduction
Alzheimer's disease (AD) is neuropathologically marked by amyloid beta (Aβ) plaques and neurofibrillary tangles. Little is known about isotopic compositions of human AD brains. Here we study this in comparison with control subjects for copper and zinc.
Methods
We use mass‐spectrometry methods, developed to study extraterrestrial materials, to compare the copper and zinc isotopic composition of 10 AD and 10 control brains.
Results
Copper and zinc natural isotopic compositions of AD brains are statistically different compared to controls, and correlate with Braak stages.
Discussion
The distribution of natural copper and zinc isotopes in AD is not affected by the diet, but is a consequence of Aβ plaques and tau fibril accumulation. This is well predicted by the changes of the chemical bonding environment caused by the development of Aβ lesions and accumulation of tau proteins. Future work will involve testing whether these changes affect brain functions and are propagated to body fluids. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Online correction added on March 02, 2022: appearance of the author's name is incorrect in the original published version. The fifth author's name was updated to read as “Francois Mouton‐Liger” |
ISSN: | 2352-8729 2352-8729 |
DOI: | 10.1002/dad2.12112 |