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Acat1 Knockdown Gene Therapy Decreases Amyloid-β in a Mouse Model of Alzheimer's Disease

Murphy, Stephanie R, Chang, Catherine CY, Dogbevia, Godwin, Bryleva, Elena Y, Bowen, Zachary, Hasan, Mazahir T, Chang, Ta-Yuan·2013·Molecular Therapy
DOI 10.1038/mt.2013.118
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  • Interventions that promote cholesterol-regulating processes reduce Aβ pathology, including increasing ER-free cholesterol via inhibiting cholesteryl ester formation by ACAT1 inhibition.

    “Interestingly, interventions that promote these processes reduce Aβ pathology, including increasing ER-FC via inhibiting CE formation by ACAT1 inhibition [74, 75, 103, 111].”

    From Inhibition of ACAT as a Therapeutic Target for Alzheimer's Disease Is Independent of ApoE4 Lipidation (2023) · cites this paper as [74]

    The Introduction states that ACAT enzymes form cholesteryl esters, and the Results (‘Testing of AAV gene therapy effects on AD mice’; page unavailable) report significantly lower Aβ42 after Acat1 knockdown in AD mice. The paper does not establish that this treatment increased ER-free cholesterol or that such an increase caused the Aβ reduction; the Discussion says the molecular mechanism remains incompletely understood. (LLM, conf=0.86)

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  • In vivo, attenuating ACAT activity increases levels of 24-hydroxycholesterol and decreases the content of APP and Aβ in the brain of FAD-Tg mice.

    “In vivo, attenuating ACAT activity increases the levels of 24-hydroxycholesterol and decreases the content of APP and Aβ in the brain of FAD-Tg mice [73, 74].”

    From Inhibition of ACAT as a Therapeutic Target for Alzheimer's Disease Is Independent of ApoE4 Lipidation (2023) · cites this paper as [74]

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Research works printed but not linked: 42

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Metadata

Authors
Murphy, S. R., Chang, C. C., Dogbevia, G., Bryleva, E. Y., Bowen, Z., Hasan, M. T., & Chang, T.-Y.
Venue
Molecular Therapy
Publisher
Elsevier BV
Published
2013-08
Volume
21
Issue
8
Pages
1497-1506
ISSN
1525-0016
DOI
10.1038/mt.2013.118
Cited by
96
References
6
Language
en
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