The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Effect of statins on Alzheimer’s disease biomarkers in cerebrospinal fluid
Abstract
Background Treatment with HMG-CoA reductase inhibitors ("statins") has been variably associated with a reduced risk of Alzheimer's disease (AD) in epidemiologic studies and reduced amyloid-beta (Abeta) deposition in animal models of AD. Putative neuroprotective effects of statins may vary in relation to their ability to penetrate into the central nervous system (CNS). Methods We measured levels of cerebrospinal fluid (CSF) AD biomarkers following 14 weeks of treatment with simvastatin (a CNS permeant statin; n=10) at 40 mg/day or pravastatin (a CNS impermeant statin; n=13) at 80 mg/day in hypercholesterolemic subjects without dementia. Results Simvastatin, but not pravastatin, reduced CSF levels of phospho-tau-181 (p-tau181) in all subjects. There were no differences in CSF levels of total tau, Abeta42, Abeta40, soluble amyloid beta protein precursor (sAbetaPP) alpha or beta, or F2-isoprostanes. Conclusions Statins may modulate the phosphorylation of tau in humans and this effect may depend on the CNS availability of the statin. These results suggest another mechanism by which statins may act to reduce the risk of AD.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
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?
Statins reduce pTau levels in CSF from AD patients.
“Statins also reduce pTau levels in CSF from AD patients (Riekse et al., 2006).”
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 Riekse et al., 2006
Increased cholesterol levels are present in tandem with neuronal dysfunction and tau aggregation in several experimental models.
“Using several experimental models, it has been shown that increased cholesterol levels are present in tandem with neuronal dysfunction and tau aggregation4,5,18–25.”
From GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau (2025) · cites this paper as [20]
Statins have been shown to reduce tau pathology in animal models of tauopathy and in CSF from AD patients.
“In addition, statins, which can lower cholesterol in some reports, has been shown to reduce tau pathology in animal models of tauopathy19 and in cerebrospinal fluid (CSF) from AD patients20.”
From GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau (2025) · cites this paper as [20]
Increases in neuronal CE drive ptau accumulation in hiPSCs-derived AD neurons; statins reduce tau pathology in animal models of tauopathy and in CSF from AD patients; and genetic inhibition of CE by ACAT1 reduces tauopathy in an AD-mouse model.
“Increases in neuronal CE drive ptau accumulation in hiPSCs-derived AD neurons18–21; while statins, a class of lipid-lowering medications, reduce tau pathology in animal models of tauopathy19 and in cerebrospinal fluid (CSF) from AD patients20, and genetic inhibition of CE by acetyl-CoA acetyltransferase 1 (ACAT1) reduces tauopathy in an AD-mouse model21.”
From GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau (2025) · cites this paper as [20]
Citations
Cites
Morris, J. C. (1997) · International Psychogeriatrics · doi:10.1017/s1041610297004870 · Cited by 1,641
Reiman, E. M., Caselli, R. J., Yun, L. S., Chen, K., Bandy, D., Minoshima, S., Thibodeau, S. N., & Osborne, D. (1996) · New England Journal of Medicine · doi:10.1056/nejm199603213341202 · Cited by 1,366
Mild cognitive impairment in the elderly: Predictors of dementia
Flicker, C., Ferris, S. H., & Reisberg, B. (1991) · Neurology · doi:10.1212/wnl.41.7.1006 · Cited by 838
Snowdon, D. A. (1996) · JAMA · doi:10.1001/jama.1996.03530310034029 · Cited by 696
P38 MAP kinase is activated at early stages in Alzheimer's disease brain
Sun, A. (2003) · Experimental Neurology · doi:10.1016/s0014-4886(03)00180-8 · Cited by 219
Flagged first, then by citations
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
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
Statins, cognition, and dementia-systematic review and methodological commentary
Power, M. C., Weuve, J., Sharrett, A. R., Blacker, D., & Gottesman, R. F. (2015) · Nature Reviews Neurology · doi:10.1038/nrneurol.2015.35 · Cited by 150
Ray, B., B. Chauhan, N., & K. Lahiri, D. (2011) · Current Medicinal Chemistry · doi:10.2174/092986711796504664 · Cited by 100
Butterfield, D. A., Barone, E., & Mancuso, C. (2011) · Pharmacological Research · doi:10.1016/j.phrs.2011.04.007 · Cited by 80
“Statins showed positive effects against Alzheimer-relevant Aβ-induced oxidative stress in mice models of AD [41,42] as well as a reduction in CSF tau protein phosphorylation in humans [43].”
BackgroundGRAMD1B 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
- Riekse, R. G., Li, G., Petrie, E. C., Leverenz, J. B., Vavrek, D., Vuletic, S., Albers, J. J., Montine, T. J., Lee, V. M.-Y., Lee, M., Seubert, P., Galasko, D., Schellenberg, G. D., Hazzard, W. R., & Peskind, E. R.
- Affiliations
- Department of Medicine, Division of Geriatric Medicine, University of Washington School of Medicine, WA, USA
- Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, WA, USA
- Northwest Network VISN-20 Mental Illness Research, Education, and Clinical Center (MIRECC), VA Puget Sound Health Care System, Seattle, WA, USA
- Northwest Lipid Metabolism and Diabetes Research Laboratories, University of Washington School of Medicine, WA, USA
- Department of Pathology, Division of Neuropathology, University of Washington School of Medicine, WA, USA
- Department of Pathology, University of Pennsylvania, Philadelphia, PA, USA
- Elan Pharmaceuticals, South San Francisco, CA, USA
- Department of Neurology, University of California, San Diego, CA, USA
- Venue
- Journal of Alzheimer's Disease
- Publisher
- SAGE Publications
- Published
- 2006-12-13
- Volume
- 10
- Issue
- 4
- Pages
- 399-406
- ISSN
- 1875-8908
- 1387-2877
- Cited by
- 90
- References
- 5
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
