Plasma lipoprotein b-amyloid in subjects with Alzheimer's disease or mild cognitive impairment
Background: Plasma amyloid -peptide (A) can compromise the blood-brain barrier, contributing to cerebrovascular alterations and amyloid angiopathy in Alzheimer's disease (AD). The objectives of this study were to investigate the distribution of lipoprotein-bound plasma-A isoforms.Methods: This...
| Main Authors: | , , , , , |
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| Format: | Journal Article |
| Published: |
Royal Society of Medicine Press Ltd
2008
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| Online Access: | http://hdl.handle.net/20.500.11937/40017 |
| _version_ | 1848755752187985920 |
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| author | Mamo, John Jian, Le James, A. Flicker, L. Esselmann, H. Wiltfang, J. |
| author_facet | Mamo, John Jian, Le James, A. Flicker, L. Esselmann, H. Wiltfang, J. |
| author_sort | Mamo, John |
| building | Curtin Institutional Repository |
| collection | Online Access |
| description | Background: Plasma amyloid -peptide (A) can compromise the blood-brain barrier, contributing to cerebrovascular alterations and amyloid angiopathy in Alzheimer's disease (AD). The objectives of this study were to investigate the distribution of lipoprotein-bound plasma-A isoforms.Methods: This involved a case-control study of subjects with AD or amnestic mild cognitive impairment (MCI) versus controls. Lipoprotein A distribution was determined in fasted plasma. For assessment of chylomicron homeostasis in the postabsorptive state, subjects were bled 4 h after a low-fat meal. The main outcome measures were plasma lipoprotein A isoform distribution and lipid homeostasis.Results: We found the majority of plasma A to be associated with triglyceride-rich lipoproteins (TRLs) encompassing chylomicrons, VLDL and IDL. For all lipoprotein groups, A1 40 was the predominant isoform, accounting for approximately 50% of the total. Thereafter, equivalent amounts of the isoforms 1 42, 2 40, 1 38, 1 37 and 1 39 were found. A1 37, A1 38 and A2 40 isoforms were significantly enriched within the TRL fraction of AD/MCI subjects and similar trends were observed for isoforms A1 39, A1 40 and A1 42. Lipoprotein-A was inversely associated with plasma total- and LDL cholesterol. AD/MCI subjects were not dyslipidaemic, however, there was evidence of accumulation of chylomicrons in the postabsorptive state.Conclusions: Our data show that A was found to be associated with plasma lipoproteins, especially those enriched with triglyceride. We find that A may be increased in normolipidaemic AD subjects, commensurate with possible disturbances in postprandial lipoprotein homeostasis. |
| first_indexed | 2025-11-14T09:01:18Z |
| format | Journal Article |
| id | curtin-20.500.11937-40017 |
| institution | Curtin University Malaysia |
| institution_category | Local University |
| last_indexed | 2025-11-14T09:01:18Z |
| publishDate | 2008 |
| publisher | Royal Society of Medicine Press Ltd |
| recordtype | eprints |
| repository_type | Digital Repository |
| spelling | curtin-20.500.11937-400172017-09-13T15:53:17Z Plasma lipoprotein b-amyloid in subjects with Alzheimer's disease or mild cognitive impairment Mamo, John Jian, Le James, A. Flicker, L. Esselmann, H. Wiltfang, J. Background: Plasma amyloid -peptide (A) can compromise the blood-brain barrier, contributing to cerebrovascular alterations and amyloid angiopathy in Alzheimer's disease (AD). The objectives of this study were to investigate the distribution of lipoprotein-bound plasma-A isoforms.Methods: This involved a case-control study of subjects with AD or amnestic mild cognitive impairment (MCI) versus controls. Lipoprotein A distribution was determined in fasted plasma. For assessment of chylomicron homeostasis in the postabsorptive state, subjects were bled 4 h after a low-fat meal. The main outcome measures were plasma lipoprotein A isoform distribution and lipid homeostasis.Results: We found the majority of plasma A to be associated with triglyceride-rich lipoproteins (TRLs) encompassing chylomicrons, VLDL and IDL. For all lipoprotein groups, A1 40 was the predominant isoform, accounting for approximately 50% of the total. Thereafter, equivalent amounts of the isoforms 1 42, 2 40, 1 38, 1 37 and 1 39 were found. A1 37, A1 38 and A2 40 isoforms were significantly enriched within the TRL fraction of AD/MCI subjects and similar trends were observed for isoforms A1 39, A1 40 and A1 42. Lipoprotein-A was inversely associated with plasma total- and LDL cholesterol. AD/MCI subjects were not dyslipidaemic, however, there was evidence of accumulation of chylomicrons in the postabsorptive state.Conclusions: Our data show that A was found to be associated with plasma lipoproteins, especially those enriched with triglyceride. We find that A may be increased in normolipidaemic AD subjects, commensurate with possible disturbances in postprandial lipoprotein homeostasis. 2008 Journal Article http://hdl.handle.net/20.500.11937/40017 10.1258/acb.2008.007214 Royal Society of Medicine Press Ltd unknown |
| spellingShingle | Mamo, John Jian, Le James, A. Flicker, L. Esselmann, H. Wiltfang, J. Plasma lipoprotein b-amyloid in subjects with Alzheimer's disease or mild cognitive impairment |
| title | Plasma lipoprotein b-amyloid in subjects with Alzheimer's disease or mild cognitive impairment |
| title_full | Plasma lipoprotein b-amyloid in subjects with Alzheimer's disease or mild cognitive impairment |
| title_fullStr | Plasma lipoprotein b-amyloid in subjects with Alzheimer's disease or mild cognitive impairment |
| title_full_unstemmed | Plasma lipoprotein b-amyloid in subjects with Alzheimer's disease or mild cognitive impairment |
| title_short | Plasma lipoprotein b-amyloid in subjects with Alzheimer's disease or mild cognitive impairment |
| title_sort | plasma lipoprotein b-amyloid in subjects with alzheimer's disease or mild cognitive impairment |
| url | http://hdl.handle.net/20.500.11937/40017 |