The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Altered cholesterol ester cycle in skin fibroblasts from patients with Alzheimer’s disease
Abstract
Intracellular cholesterol metabolism was reported to modulate amyloid-beta (Abeta) generation in Alzheimer's disease (AD). Results presented herein demonstrated that, like brain cells, cultured skin fibroblasts from AD patients contained more cholesterol esters than fibroblasts from healthy subjects. Particularly, Oil Red-O, Nile Red, and filipin staining highlighted higher levels of neutral lipids which responded to inhibitors of acyl-coenzyme A:cholesterol acyl-transferase (ACAT-1), associated with an increase in free cholesterol. ACAT-1 mRNA levels increased significantly in AD fibroblasts, whereas those of sterol regulatory element binding protein-2, neutral cholesterol ester hydrolase, and ATP-binding cassette transporter member 1 were markedly down-regulated. Instead, mRNA levels of low-density lipoprotein receptor, hydroxy-methyl-glutaryl-coenzyme A reductase, caveolin-1, and amyloid-beta protein precursor (AbetaPP) were virtually unchanged. Notably, mRNA levels of both beta-site AbetaPP-cleaving enzyme 1 (BACE1) and neprilysin were significantly down-regulated. An increase in Abeta(40) and Abeta(42) immunostaining and a decrease in BACE1 active form were also found in AD versus control fibroblasts. Altogether, these findings support the hypothesis that the derangement of cholesterol homeostasis is a systemic alteration involving central but also peripheral cells of AD patients, and point to cholesterol ester levels in AD fibroblasts as an additional metabolic hallmark…
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CE production is overactive in human SAD fibroblasts.
“Interestingly, CE production is overactive in human SAD fibroblasts (Pani et al., 2009) and APOE, the major genetic risk factor for SAD, acts as a CE transporter in brain (Liu et al., 2013, Michikawa et al., 2000, Minagawa et al., 2009).”
From Cholesterol Metabolism Is a Druggable Axis that Independently Regulates Tau and Amyloid-β in iPSC-Derived Alzheimer’s Disease Neurons (2019) · cites this paper as Pani et al., 2009
The altered gene expression and pathways revealed by MAPT R406W HNOs coincide with altered lipid metabolism and cholesterol regulation previously identified in FTLD and AD patients.
“The altered gene expression and pathways revealed by MAPT R406W HNOs coincide with altered lipid metabolism and cholesterol regulation, which has been previously identified in FTLD and AD patients6,67,68.”
From GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau (2025) · cites this paper as [67]
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Cites
Spectrofluorometric studies of the lipid probe, nile red.
Greenspan, P., & Fowler, S. D. (1985) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)34307-8 · Cited by 980
Vetrivel, K. S., Meckler, X., Chen, Y., Nguyen, P. D., Seidah, N. G., Vassar, R., Wong, P. C., Fukata, M., Kounnas, M. Z., & Thinakaran, G. (2009) · Journal of Biological Chemistry · doi:10.1074/jbc.m808920200 · Cited by 153
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Upregulated function of mitochondria‐associated ER membranes in Alzheimer disease
Area‐Gomez, E., del Carmen Lara Castillo, M., Tambini, M. D., Guardia‐Laguarta, C., de Groof, A. J. C., Madra, M., Ikenouchi, J., Umeda, M., Bird, T. D., Sturley, S. L., et al. (2012) · The EMBO Journal · doi:10.1038/emboj.2012.202 · Cited by 638
van der Kant, R., Langness, V. F., Herrera, C. M., Williams, D. A., Fong, L. K., Leestemaker, Y., Steenvoorden, E., Rynearson, K. D., Brouwers, J. F., Helms, J. B., et al. (2019) · Cell Stem Cell · doi:10.1016/j.stem.2018.12.013 · Cited by 350
GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau
Acosta Ingram, D., Turkes, E., Kim, T. Y., Vo, S., Sweeney, N., Bonte, M.-A., Rutherford, R., Julian, D. L., Pan, M., Marsh, J., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-58585-w · Cited by 12
Metadata
- Authors
- Pani, A., Dessì, S., Diaz, G., La Colla, P., Abete, C., Mulas, C., Angius, F., Cannas, M. D., Orru, C. D., Cocco, P. L., Mandas, A., Putzu, P., Laurenzana, A., Cellai, C., Costanza, A. M., Bavazzano, A., Mocali, A., & Paoletti, F.
- Affiliations
- Department of Biomedical Sciences and Technologies, University of Cagliari, Italy
- Department of Internal Medical Science, University of Cagliari, Italy
- Alzheimer Center, ASL 8, Cagliari, Italy
- Department of Experimental Pathology and Oncology, University of Florence, Italy
- Azienda ASL 4, Geriatric Unit of Prato Hospital, Prato, Italy
- Venue
- Journal of Alzheimer's Disease
- Publisher
- SAGE Publications
- Published
- 2009-11-12
- Volume
- 18
- Issue
- 4
- Pages
- 829-841
- ISSN
- 1875-8908
- 1387-2877
- Cited by
- 49
- References
- 2
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