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Brain region-specific amyloid plaque-associated myelin lipid loss, APOE deposition and disruption of the myelin sheath in familial Alzheimer's disease mice

Journal article
Authors Ibrahim Kaya
Eva Jennische
Stephan Lange
A. T. Baykal
P. Malmberg
John S. Fletcher
Published in Journal of Neurochemistry
Volume 154
Issue 1
Pages 84-98
ISSN 0022-3042
Publication year 2020
Published at Institute of Biomedicine
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Department of Chemistry and Molecular Biology
Pages 84-98
Language en
Keywords Alzheimer's disease, amyloid plaques, apolipoprotein E (APOE), MALDI, Imaging Mass Spectrometry, myelin lipids, sulfatides, imaging mass-spectrometry, central-nervous-system, apolipoprotein-e, mouse model, beta peptides, neutral sphingomyelinase, lysophosphatidyl, choline, plasmalogen deficiency, induced demyelination, microglial, response, Biochemistry & Molecular Biology, Neurosciences & Neurology
Subject categories Neurochemistry


There is emerging evidence that amyloid beta (A beta) aggregates forming neuritic plaques lead to impairment of the lipid-rich myelin sheath and glia. In this study, we examined focal myelin lipid alterations and the disruption of the myelin sheath associated with amyloid plaques in a widely used familial Alzheimer's disease (AD) mouse model; 5xFAD. This AD mouse model has A beta(42) peptide-rich plaque deposition in the brain parenchyma. Matrix-assisted laser desorption/ionization imaging mass spectrometry of coronal brain tissue sections revealed focal A beta plaque-associated depletion of multiple myelin-associated lipid species including sulfatides, galactosylceramides, and specific plasmalogen phopshatidylethanolamines in the hippocampus, cortex, and on the edges of corpus callosum. Certain phosphatidylcholines abundant in myelin were also depleted in amyloid plaques on the edges of corpus callosum. Further, lysophosphatidylethanolamines and lysophosphatidylcholines, implicated in neuroinflammation, were found to accumulate in amyloid plaques. Double staining of the consecutive sections with fluoromyelin and amyloid-specific antibody revealed amyloid plaque-associated myelin sheath disruption on the edges of the corpus callosum which is specifically correlated with plaque-associated myelin lipid loss only in this region. Further, apolipoprotein E, which is implicated in depletion of sulfatides in AD brain, is deposited in all the A beta plaques which suggest apolipoprotein E might mediate sulfatide depletion as a consequence of an immune response to A beta deposition. This high-spatial resolution matrix-assisted laser desorption/ionization imaging mass spectrometry study in combination with (immuno) fluorescence staining of 5xFAD mouse brain provides new understanding of morphological, molecular and immune signatures of A beta plaque pathology-associated myelin lipid loss and myelin degeneration in a brain region-specific manner.

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