LDL Receptor Deficiency Does not Alter Brain Amyloid-β Levels but Causes an Exacerbation of Apoptosis

de Oliveira, Jade; Engel, Daiane F.; de Paula, Gabriela C.; Melo, Helen M.; Lopes, Samantha C.; Ribeiro, Camila T.; Delanogare, Eslen; Moreira, José Claudio F.; Gelain, Daniel P.; Prediger, Rui D.; Gabilan, Nelson H.; Moreira, Eduardo Luiz G.; Ferreira, Sergio T.; de Bem, Andreza F.

doi:10.3233/jad-190742

Cited by 31Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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LDL Receptor Deficiency Does not Alter Brain Amyloid-β Levels but Causes an Exacerbation of Apoptosis

de Oliveira, Jade, Engel, Daiane F., de Paula, Gabriela C., Melo, Helen M., Lopes, Samantha C., Ribeiro, Camila T., Delanogare, Eslen, Moreira, José Claudio F., Gelain, Daniel P., Prediger, Rui D., Gabilan, Nelson H., Moreira, Eduardo Luiz G., Ferreira, Sergio T., de Bem, Andreza F.·2020·Journal of Alzheimer’s Disease

DOI 10.3233/jad-190742

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Abstract

Familial hypercholesterolemia (FH) is a genetic disorder caused by dysfunction of low density lipoprotein receptors (LDLr), resulting in elevated plasma cholesterol levels. FH patients frequently exhibit cognitive impairment, a finding recapitulated in LDLr deficient mice (LDLr -/- ), an animal model of FH. In addition, LDLr -/- mice are more vulnerable to the deleterious memory impact of amyloid-β (Aβ), a peptide linked to Alzheimer’s disease. Here, we investigated whether the expression of proteins involved in Aβ metabolism are altered in the brains of adult or middle-aged LDLr -/- mice. After spatial memory assessment, Aβ levels and gene expression of LDLr related-protein 1, proteins involved in Aβ synthesis, and apoptosis-related proteins were evaluated in prefrontal cortex and hippocampus. Moreover, the location and cell-specificity of apoptosis signals were evaluated. LDLr -/- mice presented memory impairment, which was more severe in middle-aged animals. Memory deficit in LDLr -/- mice was not associated with altered expression of proteins involved in Aβ processing or changes in Aβ levels in either hippocampus or prefrontal cortex. We further found that the expression of Bcl-2 was reduced while the expression of Bax was increased in both prefrontal cortex and hippocampus in 3- and 14-month-old LDLr -/- mice Finally, LDLr -/- mice presented increased immunoreactivity for activated caspase-3 in the prefrontal cortex and hippocampus. The activation of caspase 3 was predominantly associated with neurons in LDLr -/- mice. Cognitive impairment in LDLr -/- mice is thus accompanied by an exacerbation of neuronal apoptosis in brain regions related to memory formation, but not by changes in Aβ processing or levels.

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Silencing of lipoprotein receptors implicated in cholesterol uptake and targeted by PCSK9 led to cognitive impairment in in vivo animal studies, likely related to neuronal loss.
“On the other hand, the cholesterol depletion hypothesis is in full accordance with the results of in vivo animal studies, in which silencing of lipoprotein receptors, implicated in cholesterol uptake and target of PCSK9, led to cognitive impairment [55,56,57,58,59], which was likely related to neuronal loss.”
From PCSK9 affects astrocyte cholesterol metabolism and reduces neuron cholesterol supplying in vitro: potential implications in Alzheimer’s disease (2022) · cites this paper as [58]
Cognitive impairment observed in LDLr−/− mice was associated with neuronal apoptosis in brain regions related to memory formation.
“Notably, as reported by Oliveira J. et al., the cognitive impairment observed in LDLr−/− mice was associated with neuronal apoptosis in brain regions related to memory formation [58].”
From PCSK9 affects astrocyte cholesterol metabolism and reduces neuron cholesterol supplying in vitro: potential implications in Alzheimer’s disease (2022) · cites this paper as [58]

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Cites a retracted work: 10.1016/j.expneurol.2006.03.019
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Cited work 10.1016/j.expneurol.2006.03.019 · retracted 2006-08-01 · notice 10.1016/j.expneurol.2006.03.019 · this paper published 2019-12-02
Cites a retracted work: 10.1016/j.nbd.2008.08.002
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Mechanisms underlying cognitive impairment in a mouse model of familial hypercholesterolemia: Evidences of LDLr ‐/‐ mice
Rodrigues, M. S., de Oliveira, J., Engel, D. F., de Paula, G. C., Melo, H. M., Lopes, S. C., Ribeiro, C. T., Machado, A. G., Bast, R. K., Moreira, J. C. F., et al. (2021) · Alzheimer s & Dementia · doi:10.1002/alz.051539
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Increased Susceptibility to Amyloid-β-Induced Neurotoxicity in Mice Lacking the Low-Density Lipoprotein Receptor
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Beyond cardiovascular risk: Implications of Familial hypercholesterolemia on cognition and brain function
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Authors: de Oliveira, J., Engel, D. F., de Paula, G. C., Melo, H. M., Lopes, S. C., Ribeiro, C. T., Delanogare, E., Moreira, J. C. F., Gelain, D. P., Prediger, R. D., Gabilan, N. H., Moreira, E. L. G., Ferreira, S. T., & de Bem, A. F.
Affiliations: Universidade Federal do Rio Grande do Sul (BR)
Universidade Federal de Santa Catarina (BR)
Universidade Federal do Rio de Janeiro (BR)
Programa de Pós-Graduação em Ciências Biológicas: Bioquímica, Departamento de Bioquímica, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brasil
Departamento de Bioquímica, Universidade Federal de Santa Catarina, Florianópolis, SC, Brasil
Corresponding author: de Oliveira, Jade
ORCID: de Oliveira, Jade
Engel, Daiane F.
de Paula, Gabriela C.
Melo, Helen M.
Lopes, Samantha C.
Ribeiro, Camila T.
Delanogare, Eslen
Gelain, Daniel P.
Prediger, Rui D.
Moreira, Eduardo Luiz G.
Ferreira, Sergio T.
Venue: Journal of Alzheimer’s Disease
Publisher: SAGE Publications
Published: 2019-12-02
Volume: 73
Issue: 2
Pages: 585-596
ISSN: 1387-2877 (ISSN-L)
1875-8908
DOI: 10.3233/jad-190742
OpenAlex: W2992119391
Cited by: 31
References: 36
Citations by year: 2026: 5 · 2025: 6 · 2024: 2 · 2023: 8 · 2022: 5 · 2021: 4 · 2020: 1
FWCI: 0.99
Type: journal article
Language: en
Open access: closed
Licence: journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
Locations: Journal of Alzheimer s Disease (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: LDL receptor deficiency, familial hypercholesterolemia
MeSH terms: Aging, Animals, Brain Chemistry, Cholesterol, Hippocampus, Male, Mice, Inbred C57BL, Receptors, LDL, Gene Expression, Amyloid beta-Protein Precursor, Apoptosis, Prefrontal Cortex, Mice, Knockout, Maze Learning, Mice, Caspase 3

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LDL Receptor Deficiency Does not Alter Brain Amyloid-β Levels but Causes an Exacerbation of Apoptosis

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