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001     165137
005     20250127111046.0
024 7 _ |a pmc:PMC9851747
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024 7 _ |a 10.1093/hmg/ddac205
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024 7 _ |a pmid:36001352
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024 7 _ |a 0964-6906
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024 7 _ |a 1460-2083
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037 _ _ |a DZNE-2022-01442
041 _ _ |a English
082 _ _ |a 570
100 1 _ |a Kilzheimer, Alexander
|b 0
245 _ _ |a Failure of diet-induced transcriptional adaptations in alpha-synuclein transgenic mice.
260 _ _ |a Oxford
|c 2023
|b Oxford Univ. Press
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500 _ _ |a CC BY: https://creativecommons.org/licenses/by/4.0/
520 _ _ |a Nutritional influences have been discussed as potential modulators of Parkinson's disease (PD) pathology through various epidemiological and physiological studies. In animal models, a high-fat diet (HFD) with greater intake of lipid-derived calories leads to accelerated disease onset and progression. The underlying molecular mechanisms of HFD-induced aggravated pathology, however, remain largely unclear. In this study, we aimed to further illuminate the effects of a fat-enriched diet in PD by examining the brainstem and hippocampal transcriptome of alpha-synuclein transgenic mice exposed to a life-long HFD. Investigating individual transcript isoforms, differential gene expression and co-expression clusters, we observed that transcriptional differences between wild-type (WT) and transgenic animals intensified in both regions under HFD. Both brainstem and hippocampus displayed strikingly similar transcriptomic perturbation patterns. Interestingly, expression differences resulted mainly from responses in WT animals to HFD, while these genes remained largely unchanged or were even slightly oppositely regulated by diet in transgenic animals. Genes and co-expressed gene groups exhibiting this dysregulation were linked to metabolic and mitochondrial pathways. Our findings propose the failure of metabolic adaptions as the potential explanation for accelerated disease unfolding under exposure to HFD. From the identified clusters of co-expressed genes, several candidates lend themselves to further functional investigations.
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650 _ 7 |a alpha-Synuclein
|2 NLM Chemicals
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Mice, Transgenic
|2 MeSH
650 _ 2 |a alpha-Synuclein: genetics
|2 MeSH
650 _ 2 |a alpha-Synuclein: metabolism
|2 MeSH
650 _ 2 |a Parkinson Disease: genetics
|2 MeSH
650 _ 2 |a Parkinson Disease: metabolism
|2 MeSH
650 _ 2 |a Diet, High-Fat: adverse effects
|2 MeSH
650 _ 2 |a Gene Expression Profiling
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
700 1 _ |a Hentrich, Thomas
|b 1
700 1 _ |a Rotermund, Carola
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700 1 _ |a Kahle, Philipp J
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700 1 _ |a Schulze-Hentrich, Julia M
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773 _ _ |a 10.1093/hmg/ddac205
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|t Human molecular genetics
|v 32
|y 2023
|x 0964-6906
856 4 _ |u https://pub.dzne.de/record/165137/files/DZNE-2022-01442.pdf
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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