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The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

Cholesterol 24-hydroxylase defect is implicated in memory impairments associated with Alzheimer-like Tau pathology

Burlot, Marie-Anne, Braudeau, Jérôme, Michaelsen-Preusse, Kristin, Potier, Brigitte, Ayciriex, Sophie, Varin, Jennifer, Gautier, Benoit, Djelti, Fathia, Audrain, Mickael, Dauphinot, Luce, Fernandez-Gomez, Francisco-Jose, Caillierez, Raphaëlle, Laprévote, Olivier, Bièche, Ivan, Auzeil, Nicolas, Potier, Marie-Claude, Dutar, Patrick, Korte, Martin, Buée, Luc, Blum, David, Cartier, Nathalie·2015·Human Molecular Genetics
DOI 10.1093/hmg/ddv268
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Abstract

Alzheimer's disease (AD) is characterized by both amyloid and Tau pathologies. The amyloid component and altered cholesterol metabolism are closely linked, but the relationship between Tau pathology and cholesterol is currently unclear. Brain cholesterol is synthesized in situ and cannot cross the blood-brain barrier: to be exported from the central nervous system into the blood circuit, excess cholesterol must be converted to 24S-hydroxycholesterol by the cholesterol 24-hydroxylase encoded by the CYP46A1 gene. In AD patients, the concentration of 24S-hydroxycholesterol in the plasma and the cerebrospinal fluid are lower than in healthy controls. The THY-Tau22 mouse is a model of AD-like Tau pathology without amyloid pathology. We used this model to investigate the potential association between Tau pathology and CYP46A1 modulation. The amounts of CYP46A1 and 24S-hydroxycholesterol in the hippocampus were lower in THY-Tau22 than control mice. We used an adeno-associated virus (AAV) gene transfer strategy to increase CYP46A1 expression in order to investigate the consequences on THY-Tau22 mouse phenotype. Injection of the AAV-CYP46A1 vector into the hippocampus of THY-Tau22 mice led to CYP46A1 and 24S-hydroxycholesterol content normalization. The cognitive deficits, impaired long-term depression and spine defects that characterize the THY-Tau22 model were completely rescued, whereas Tau hyperphosphorylation and associated gliosis were unaffected. These results argue for a causa…

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Research works printed but not linked: 57

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Metadata

Authors
Burlot, M.-A., Braudeau, J., Michaelsen-Preusse, K., Potier, B., Ayciriex, S., Varin, J., Gautier, B., Djelti, F., Audrain, M., Dauphinot, L., Fernandez-Gomez, F.-J., Caillierez, R., Laprévote, O., Bièche, I., Auzeil, N., Potier, M.-C., Dutar, P., Korte, M., Buée, L., Blum, D., & Cartier, N.
Venue
Human Molecular Genetics
Publisher
Oxford University Press (OUP)
Published
2015-09-10
Volume
24
Issue
21
Pages
5965-5976
ISSN
  • 0964-6906
  • 1460-2083
DOI
10.1093/hmg/ddv268
Cited by
130
References
9
Language
en

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