The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Mild hypercholesterolemia is an early risk factor for the development of Alzheimer amyloid pathology
Abstract
Background Epidemiologic and experimental data suggest that cholesterol may play a role in the pathogenesis of AD. Modulation of cholesterolemia in transgenic animal models of AD strongly alters amyloid pathology. Objective To determine whether a relationship exists between amyloid deposition and total cholesterolemia (TC) in the human brain. Methods The authors reviewed autopsy cases of patients older than 40 years and correlated cholesterolemia and presence or absence of amyloid deposition (amyloid positive vs amyloid negative subjects) and cholesterolemia and amyloid load. Amyloid load in human brains was measured by immunohistochemistry and image analysis. To remove the effect of apoE isoforms on cholesterol levels, cases were genotyped and duplicate analyses were performed on apoE3/3 subjects. Results Cholesterolemia correlates with presence of amyloid deposition in the youngest subjects (40 to 55 years) with early amyloid deposition (diffuse type of senile plaques) (p = 0.000 for all apoE isoforms; p = 0.009 for apoE3/3 subjects). In this group, increases in cholesterolemia from 181 to 200 almost tripled the odds for developing amyloid, independent of apoE isoform. A logistic regression model showed consistent results (McFadden rho2 = 0.445). The difference in mean TC between subjects with and without amyloid disappeared as the age of the sample increased (>55 years: p = 0.491), possibly reflecting the effect of cardiovascular deaths among other possibilities. TC and am…
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?
High midlife plasma total cholesterol levels are associated with an increased risk of Alzheimer's disease.
“Epidemiological studies suggest that high midlife plasma total cholesterol levels are associated with an increased risk of AD.”
From ApoB100/LDLR-/- Hypercholesterolaemic Mice as a Model for Mild Cognitive Impairment and Neuronal Damage (2011) · cites this paper as [2]
Hypercholesterolaemia is an early risk factor for Alzheimer's disease.
“Epidemiological studies have shown that hypercholesterolaemia is an early (rather than a late) risk factor for AD, and that elevated plasma concentrations of LDL cholesterol correlate well with the appearance of AD [1], [2], [3], [4].”
From ApoB100/LDLR-/- Hypercholesterolaemic Mice as a Model for Mild Cognitive Impairment and Neuronal Damage (2011) · cites this paper as [2]
Hypercholesterolaemia may be an early risk factor for AD.
“Patients with FH are exposed to higher cholesterol levels from birth, and it is reported that hypercholesterolaemia may be an early risk factor for AD [2], [4].”
From ApoB100/LDLR-/- Hypercholesterolaemic Mice as a Model for Mild Cognitive Impairment and Neuronal Damage (2011) · cites this paper as [2]
Individuals with elevated midlife plasma cholesterol are at increased risk of dementia and AD.
“Clinical and epidemiological evidence suggest that individuals with elevated midlife plasma cholesterol are at increased risk of dementia and AD [1], [2], [3], [4].”
From ApoB100/LDLR-/- Hypercholesterolaemic Mice as a Model for Mild Cognitive Impairment and Neuronal Damage (2011) · cites this paper as [2]
Patients with FH are exposed to higher cholesterol levels from birth.
“Patients with FH are exposed to higher cholesterol levels from birth, and it is reported that hypercholesterolaemia may be an early risk factor for AD [2], [4].”
From ApoB100/LDLR-/- Hypercholesterolaemic Mice as a Model for Mild Cognitive Impairment and Neuronal Damage (2011) · cites this paper as [2]
Patients with familial hypercholesterolaemia show a particularly high incidence of mild cognitive impairment.
“Patients with familial hypercholesterolaemia (FH) show a particularly high incidence of mild cognitive impairment (MCI), a prodromal stage of abnormal cognitive performance which precedes AD [2], [4].”
From ApoB100/LDLR-/- Hypercholesterolaemic Mice as a Model for Mild Cognitive Impairment and Neuronal Damage (2011) · cites this paper as [2]
Elevated plasma LDL cholesterol concentrations correlate with the appearance of Alzheimer's disease.
“Epidemiological studies have shown that hypercholesterolaemia is an early (rather than a late) risk factor for AD, and that elevated plasma concentrations of LDL cholesterol correlate well with the appearance of AD [1], [2], [3], [4].”
From ApoB100/LDLR-/- Hypercholesterolaemic Mice as a Model for Mild Cognitive Impairment and Neuronal Damage (2011) · cites this paper as [2]
Citations
Cites
Hosmer, D. W., & Lemeshow, S. (2000) · doi:10.1002/0471722146 · Cited by 20,302
Correlation Between Elevated Levels of Amyloid β-Peptide in the Brain and Cognitive Decline
Näslund, J. (2000) · JAMA · doi:10.1001/jama.283.12.1571 · Cited by 1,268
Flagged first, then by citations
Research works printed but not linked: 42
- 10.1016/S0733-8619(05)70232-2 · DOI
- 10.1001/archneur.57.10.1439 · DOI
- 10.1016/S0140-6736(00)03155-X · DOI
- 10.1007/s11745-999-0357-9 · DOI
- 10.3109/13506129909007315 · DOI
- 10.3233/JAD-1999-14-501 · DOI
- 10.1074/jbc.271.8.4436 · DOI · Paper page
- 10.1097/00001756-199906030-00014 · DOI
- 10.1073/pnas.95.11.6460 · DOI
- 10.1016/S0005-2736(98)00097-2 · DOI
- 10.1002/1097-0029(20000815)50:4<287::AID-JEMT7>3.0.CO;2-L · DOI
- 10.1006/nbdi.2000.0304 · DOI · Paper page
- 10.1111/j.1749-6632.1997.tb48466.x · DOI
- 10.1016/0197-4580(92)90116-F · DOI
- 10.1093/oxfordjournals.aje.a116417 · DOI
- 10.1159/000026149 · DOI
- Zlokovic BV, Yamada S, Holtzman D, Ghiso J, Frangione B. Clearance of amyloid beta-peptide from brain: transport or metabolism? Nat Med . 2000; 6: 718.
- 10.1212/WNL.41.4.479 · DOI · Paper page
- Pappolla MA Robakis NK. Neuropathology and molecular biology of Alzheimer’s disease. In: Stein M Baum M eds. Perspectives in behavioral medicine: Alzheimer’s disease. San Diego: Academic Press 1995; 3–20.
- Pappolla MA, Omar RA, Vinters HV. Image analysis microspectroscopy shows that neurons participate in the genesis of a subset in early primitive (diffuse) senile plaques. Am J Pathol . 1991; 139: 599–607.
- Pappolla MA, Omar RA, Sambamurti K, Anderson JP, Robakis NK. The genesis of the senile plaque. Part II. Further evidence in support of its neuronal origin. Am J Pathol . 1992; 141: 1151–1159.
- Pappolla MA. Amyloid deposition in diffuse plaques may or may not start at the neuronal cell surface membrane. J Neuropathol Exp Neurol . 2001; 60: 105–106.
- 10.1111/j.1365-2990.1986.tb00677.x · DOI
- 10.1093/ajcp/75.6.816 · DOI
- Pappolla MA. Computerized image-analysis microspectroscopy of tissue sections. Arch Pathol Lab Med . 1988; 112: 787–790.
- 10.1006/nbdi.2001.0422 · DOI
- Gironès X Chyan Y-J Riutort N et al. Macrophage activation and cell death in Alzheimer’s disease: effects of age and apolipoprotein E genotype. J Alzheimer Dis 2003 (in press).
- Holm S. A simple sequentially rejective multiple test procedure. Scand J Stat . 1979; 6: 65–70.
- Hommel G. A stagewise rejective multiple test procedure based on a modified Bonferroni test. Second edition. Biometrika . 2000; 75: 383–386.
- Ehrenberg ASC ed. Data reduction. New York: John Wiley & Sons 1975.
- 10.1001/jama.1992.03480010078028 · DOI
- 10.1161/01.ATV.12.4.416 · DOI
- 10.1093/clinchem/30.3.404 · DOI
- 10.1093/oxfordjournals.aje.a116977 · DOI
- 10.1016/0021-9681(82)90111-4 · DOI
- 10.1001/jama.280.24.2099 · DOI
- 10.1016/S0021-9150(98)90209-X · DOI
- Hensher DA Johnson LW. Applies discrete choice modeling. New York: Halsted Press/John Wiley 1981.
- 10.1212/WNL.45.6.1092 · DOI
- 10.1212/WNL.54.1.240 · DOI
- 10.1212/WNL.53.3.517 · DOI
- 10.7326/0003-4819-137-1-200207020-00006 · DOI · Paper page
Cited by
Sorted by citations
Resveratrol: French Paradox Revisited
Catalgol, B., Batirel, S., Taga, Y., & Ozer, N. K. (2012) · Frontiers in Pharmacology · doi:10.3389/fphar.2012.00141 · Cited by 449
Lack of ABCA1 Considerably Decreases Brain ApoE Level and Increases Amyloid Deposition in APP23 Mice
Koldamova, R., Staufenbiel, M., & Lefterov, I. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m504513200 · Cited by 350
Oblak, A. L., Lin, P. B., Kotredes, K. P., Pandey, R. S., Garceau, D., Williams, H. M., Uyar, A., O’Rourke, R., O’Rourke, S., Ingraham, C., et al. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.713726 · Cited by 325
Bennett, R. E., Robbins, A. B., Hu, M., Cao, X., Betensky, R. A., Clark, T., Das, S., & Hyman, B. T. (2018) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1710329115 · Cited by 299
Cardiovascular risk factors and dementia
Fillit, H., Nash, D. T., Rundek, T., & Zuckerman, A. (2008) · The American Journal of Geriatric Pharmacotherapy · doi:10.1016/j.amjopharm.2008.06.004 · Cited by 225
Cholesterol and Alzheimer’s Disease; From Risk Genes to Pathological Effects
Feringa, F. M., & van der Kant, R. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.690372 · Cited by 226
Cerebrovascular lesions induce transient -amyloid deposition
Garcia-Alloza, M., Gregory, J., Kuchibhotla, K. V., Fine, S., Wei, Y., Ayata, C., Frosch, M. P., Greenberg, S. M., & Bacskai, B. J. (2011) · Brain · doi:10.1093/brain/awr300 · Cited by 187
Gene-environment interactions in Alzheimer's disease: A potential path to precision medicine
Eid, A., Mhatre, I., & Richardson, J. R. (2019) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2019.03.005 · Cited by 164
Alzheimer’s disease, cerebrovascular disease, and the β-amyloid cascade
Honjo, K., Black, S. E., & Verhoeff, N. P. L. G. (2012) · Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques · doi:10.1017/s0317167100015547 · Cited by 152
Cholesterol, APOE genotype, and Alzheimer disease: An epidemiologic study of Nigerian Yoruba
Hall, K., Murrell, J., Ogunniyi, A., Deeg, M., Baiyewu, O., Gao, S., Gureje, O., Dickens, J., Evans, R., Smith-Gamble, V., et al. (2006) · Neurology · doi:10.1212/01.wnl.0000194507.39504.17 · Cited by 128
Circulating Biomarkers of Cognitive Decline and Dementia
Solfrizzi, V., D'Introno, A., Colacicco, A. M., Capurso, C., Todarello, O., Pellicani, V., Capurso, S. A., Pietrarossa, G., Santamato, V., Capurso, A., et al. (2006) · Clinica Chimica Acta · doi:10.1016/j.cca.2005.06.015 · Cited by 120
APP Function and Lipids: A Bidirectional Link
Grimm, M. O. W., Mett, J., Grimm, H. S., & Hartmann, T. (2017) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2017.00063 · Cited by 104
García-Morales, V., González-Acedo, A., Melguizo-Rodríguez, L., Pardo-Moreno, T., Costela-Ruiz, V. J., Montiel-Troya, M., & Ramos-Rodríguez, J. J. (2021) · Biomedicines · doi:10.3390/biomedicines9121910 · Cited by 104
Alzheimer's disease--a dysfunction in cholesterol and lipid metabolism
Lukiw, W. J., Pappolla, M., Pelaez, R. P., & Bazan, N. G. (2005) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-005-4010-6 · Cited by 59
Self-citationGonzález-Domínguez, R., García-Barrera, T., Vitorica, J., & Gómez-Ariza, J. L. (2015) · Biochimie · doi:10.1016/j.biochi.2015.01.005 · Cited by 49
Ramírez, C., Sierra, S., Tercero, I., Vázquez, J. A., Pineda, A., Manrique, T., & Burgos, J. S. (2011) · PLoS ONE · doi:10.1371/journal.pone.0022712 · Cited by 31
Vorobyeva, A. G., Lee, R., Miller, S., Longen, C., Sharoni, M., Kandelwal, P. J., Kim, F. J., Marenda, D. R., & Saunders, A. J. (2014) · Journal of Biological Chemistry · doi:10.1074/jbc.m114.591792 · Cited by 16
Metadata
- Authors
- Pappolla, M. A., Bryant-Thomas, T. K., Herbert, D., Pacheco, J., Fabra Garcia, M., Manjon, M., Girones, X., Henry, T. L., Matsubara, E., Zambon, D., Wolozin, B., Sano, M., Cruz-Sanchez, F. F., Thal, L. J., Petanceska, S. S., & Refolo, L. M.
- Affiliations
- *Co-last authors.
- Venue
- Neurology
- Published
- 2003-07-22
- Volume
- 61
- Issue
- 2
- Pages
- 199-205
- ISSN
- 0028-3878
- 1526-632X
- Cited by
- 247
- References
- 2
- 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