The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
ACAT as a Drug Target for Alzheimer’s Disease
Abstract
Accumulation of β-amyloid peptide (Aβ) in the brain regions responsible for memory and cognitive functions is a neuropathological hallmark of Alzheimer’s disease. Cholesterol may be involved in many aspects of Aβmetabolism. It affects generation, aggregation and clearance of Aβin the brain. Not only the amount but also the distribution of cholesterol within cells appears to modulate Aβbiogenesis. ACAT is an enzyme that regulates subcellular cholesterol distribution by converting membrane cholesterol to cholesteryl esters for storage and transport. We have used various cell- and animal based models to show that inhibition of ACAT strongly reduces Aβgeneration and protects from amyloid pathology. Here, we discuss data supporting ACAT inhibition as a strategy to treat Alzheimer’s disease.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
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 [111]
The paper’s discussion of ACAT inhibition (pp. 212–214) says ACAT is an ER-resident enzyme that converts free cholesterol to cholesteryl esters, and reports that inhibiting ACAT reduces Aβ generation and amyloid pathology in cell and animal models. It says inhibition changes the distribution of free and esterified cholesterol, but does not specifically establish an increase in ER free cholesterol. (LLM, conf=0.84)
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Systematic meta-analyses of Alzheimer disease genetic association studies: the AlzGene database
Bertram, L., McQueen, M. B., Mullin, K., Blacker, D., & Tanzi, R. E. (2007) · Nature Genetics · doi:10.1038/ng1934 · Cited by 1,857
Statins as a newly recognized type of immunomodulator.
Kwak, B., Mulhaupt, F., Myit, S., & Mach, F. (2000) · Nature Medicine · doi:10.1038/82219 · Cited by 1,383
Modulation of Statin-Activated Shedding of Alzheimer APP Ectodomain by ROCK
Pedrini, S., Carter, T. L., Prendergast, G., Petanceska, S., Ehrlich, M. E., & Gandy, S. (2005) · PLoS Medicine · doi:10.1371/journal.pmed.0020018 · Cited by 154
Flagged first, then by citations
Research works printed but not linked: 13
- 10.1016%2FS0140-6736%2800%2903155-X · DOI
- 10.1001%2Farchneur.57.10.1439 · DOI
- 10.1016%2FS0197-4580%2800%2900124-X · DOI · Paper page
- 10.1038%2Fnrn1652 · DOI
- 10.1523%2FJNEUROSCI.2544-04.2005 · DOI
- 10.1146%2Fannurev.biochem.66.1.613 · DOI · Paper page
- 10.1097%2F00041433-200106000-00008 · DOI
- 10.1038%2Fncb1001-905 · DOI · Paper page
- 10.1038%2Fsj.mp.4001296 · DOI
- 10.2174%2F1389557033487890 · DOI
- 10.1016%2Fj.neuron.2004.08.043 · DOI · Paper page
- 10.1358%2Fmf.2004.26.7.863738 · DOI
- 10.1016%2Fj.febslet.2007.03.056 · DOI
Cited by
Sorted by citations
Amyloid-β-independent regulators of tau pathology in Alzheimer disease
van der Kant, R., Goldstein, L. S. B., & Ossenkoppele, R. (2020) · Nature reviews. Neuroscience · doi:10.1038/s41583-019-0240-3 · Cited by 580
Parallel findings in age-related macular degeneration and Alzheimer’s disease
Ohno-Matsui, K. (2011) · Progress in Retinal and Eye Research · doi:10.1016/j.preteyeres.2011.02.004 · Cited by 280
Microdomains, Inflammation, and Atherosclerosis
Sorci-Thomas, M. G., & Thomas, M. J. (2016) · Circulation Research · doi:10.1161/circresaha.115.306246 · Cited by 165
Varma, V. R., Büşra Lüleci, H., Oommen, A. M., Varma, S., Blackshear, C. T., Griswold, M. E., An, Y., Roberts, J. A., O’Brien, R., Pletnikova, O., et al. (2021) · npj Aging and Mechanisms of Disease · doi:10.1038/s41514-021-00064-9 · Cited by 153
Valencia-Olvera, A. C., Balu, D., Faulk, N., Amiridis, A., Wang, Y., Pham, C., Avila-Munoz, E., York, J. M., Thatcher, G. R. J., & LaDu, M. J. (2023) · Neurotherapeutics · doi:10.1007/s13311-023-01375-3 · Cited by 22
Metadata
- Authors
- Huttunen, H. J., & Kovacs, D. M.
- Venue
- Neurodegenerative Diseases
- Publisher
- S. Karger AG
- Published
- 2008
- Volume
- 5
- Issue
- 3-4
- Pages
- 212-214
- ISSN
- 1660-2854
- 1660-2862
- Cited by
- 43
- References
- 3
- Language
- en
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
