Peripheral metabolism of lipoprotein-amyloid beta as a risk factor for Alzheimer's disease: potential interactive effects of APOE genotype with dietary fats
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder pathologically characterized by brain parenchymal abundance of amyloid-beta (Aβ) and the accumulation of lipofuscin material that is rich in neutral lipids. However, the mechanisms for aetiology of AD are presently not established....
| Main Authors: | , , , , , |
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| Format: | Journal Article |
| Language: | English |
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Springer Nature
2023
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| Subjects: | |
| Online Access: | http://hdl.handle.net/20.500.11937/90702 |
| _version_ | 1848765414280003584 |
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| author | D'Alonzo, Zachary Lam, Virginie Takechi, Ryu Nesbit, Michael Vaccarezza, Mauro Mamo, John |
| author_facet | D'Alonzo, Zachary Lam, Virginie Takechi, Ryu Nesbit, Michael Vaccarezza, Mauro Mamo, John |
| author_sort | D'Alonzo, Zachary |
| building | Curtin Institutional Repository |
| collection | Online Access |
| description | Alzheimer’s disease (AD) is a progressive neurodegenerative disorder pathologically characterized by brain parenchymal abundance of amyloid-beta (Aβ) and the accumulation of lipofuscin material that is rich in neutral lipids. However, the mechanisms for aetiology of AD are presently not established. There is increasing evidence that metabolism of lipoprotein-Aβ in blood is associated with AD risk, via a microvascular axis that features breakdown of the blood-brain barrier, extravasation of lipoprotein-Aβ to brain parenchyme and thereafter heightened inflammation. A peripheral lipoprotein-Aβ/capillary axis for AD reconciles alternate hypotheses for a vascular, or amyloid origin of disease, with amyloidosis being probably consequential. Dietary fats may markedly influence the plasma abundance of lipoprotein-Aβ and by extension AD risk. Similarly, apolipoprotein E (Apo E) serves as the primary ligand by which lipoproteins are cleared from plasma via high-affinity receptors, for binding to extracellular matrices and thereafter for uptake of lipoprotein-Aβ via resident inflammatory cells. The epsilon APOE ε4 isoform, a major risk factor for AD, is associated with delayed catabolism of lipoproteins and by extension may increase AD risk due to increased exposure to circulating lipoprotein-Aβ and microvascular corruption. |
| first_indexed | 2025-11-14T11:34:52Z |
| format | Journal Article |
| id | curtin-20.500.11937-90702 |
| institution | Curtin University Malaysia |
| institution_category | Local University |
| language | English |
| last_indexed | 2025-11-14T11:34:52Z |
| publishDate | 2023 |
| publisher | Springer Nature |
| recordtype | eprints |
| repository_type | Digital Repository |
| spelling | curtin-20.500.11937-907022023-04-03T02:51:45Z Peripheral metabolism of lipoprotein-amyloid beta as a risk factor for Alzheimer's disease: potential interactive effects of APOE genotype with dietary fats D'Alonzo, Zachary Lam, Virginie Takechi, Ryu Nesbit, Michael Vaccarezza, Mauro Mamo, John Dementia Alzheimer's disease, Dementia, Va;scular, Lipoprotein, ApoE, Alzheimer’s disease (AD) is a progressive neurodegenerative disorder pathologically characterized by brain parenchymal abundance of amyloid-beta (Aβ) and the accumulation of lipofuscin material that is rich in neutral lipids. However, the mechanisms for aetiology of AD are presently not established. There is increasing evidence that metabolism of lipoprotein-Aβ in blood is associated with AD risk, via a microvascular axis that features breakdown of the blood-brain barrier, extravasation of lipoprotein-Aβ to brain parenchyme and thereafter heightened inflammation. A peripheral lipoprotein-Aβ/capillary axis for AD reconciles alternate hypotheses for a vascular, or amyloid origin of disease, with amyloidosis being probably consequential. Dietary fats may markedly influence the plasma abundance of lipoprotein-Aβ and by extension AD risk. Similarly, apolipoprotein E (Apo E) serves as the primary ligand by which lipoproteins are cleared from plasma via high-affinity receptors, for binding to extracellular matrices and thereafter for uptake of lipoprotein-Aβ via resident inflammatory cells. The epsilon APOE ε4 isoform, a major risk factor for AD, is associated with delayed catabolism of lipoproteins and by extension may increase AD risk due to increased exposure to circulating lipoprotein-Aβ and microvascular corruption. 2023 Journal Article http://hdl.handle.net/20.500.11937/90702 10.1186/s12263-023-00722-5 English http://creativecommons.org/licenses/by/4.0/ Springer Nature fulltext |
| spellingShingle | Dementia Alzheimer's disease, Dementia, Va;scular, Lipoprotein, ApoE, D'Alonzo, Zachary Lam, Virginie Takechi, Ryu Nesbit, Michael Vaccarezza, Mauro Mamo, John Peripheral metabolism of lipoprotein-amyloid beta as a risk factor for Alzheimer's disease: potential interactive effects of APOE genotype with dietary fats |
| title | Peripheral metabolism of lipoprotein-amyloid beta as a risk factor for Alzheimer's disease: potential interactive effects of APOE genotype with dietary fats |
| title_full | Peripheral metabolism of lipoprotein-amyloid beta as a risk factor for Alzheimer's disease: potential interactive effects of APOE genotype with dietary fats |
| title_fullStr | Peripheral metabolism of lipoprotein-amyloid beta as a risk factor for Alzheimer's disease: potential interactive effects of APOE genotype with dietary fats |
| title_full_unstemmed | Peripheral metabolism of lipoprotein-amyloid beta as a risk factor for Alzheimer's disease: potential interactive effects of APOE genotype with dietary fats |
| title_short | Peripheral metabolism of lipoprotein-amyloid beta as a risk factor for Alzheimer's disease: potential interactive effects of APOE genotype with dietary fats |
| title_sort | peripheral metabolism of lipoprotein-amyloid beta as a risk factor for alzheimer's disease: potential interactive effects of apoe genotype with dietary fats |
| topic | Dementia Alzheimer's disease, Dementia, Va;scular, Lipoprotein, ApoE, |
| url | http://hdl.handle.net/20.500.11937/90702 |