APOE genotype and brain amyloid are associated with changes in the plasma proteome in elderly subjects without dementia
Objective Recent work has bolstered the possibility that peripheral changes may be relevant to Alzheimer's disease pathogenesis in the brain. While age‐associated blood‐borne proteins have been targeted to restore function to the aged brain, it remains unclear whether other dysfunctional system...
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| Published in | Annals of clinical and translational neurology Vol. 12; no. 2; pp. 366 - 382 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
John Wiley & Sons, Inc
01.02.2025
John Wiley and Sons Inc Wiley |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Objective
Recent work has bolstered the possibility that peripheral changes may be relevant to Alzheimer's disease pathogenesis in the brain. While age‐associated blood‐borne proteins have been targeted to restore function to the aged brain, it remains unclear whether other dysfunctional systemic states can be exploited for similar benefits. Here, we investigate whether APOE allelic variation or presence of brain amyloid are associated with plasma proteomic changes and the molecular processes associated with these changes.
Methods
Using the SOMAscan assay, we measured 1305 plasma proteins from 53 homozygous, APOE3 and APOE4 subjects without dementia. We investigated the relationship of either the APOE‐ε4 allele or amyloid positivity with plasma proteome changes by linear mixed effects modeling and ontology‐based pathway and module–trait correlation analyses.
Results
APOE4 is associated with plasma protein differences linked to atherosclerosis, tyrosine kinase activity, cholesterol transport, extracellular matrix, and synaptogenesis pathways. Independent of APOE4, we found that subjects likely harboring brain amyloid exhibit plasma proteome signatures associated with AD‐linked pathways, including neurovascular dysfunction.
Interpretation
Our results indicate that APOE4 status or presence of brain amyloid are associated with plasma proteomic shifts prior to the onset of symptoms, suggesting that systemic pathways in certain risk contexts may be plausible targets for disease modification. |
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| AbstractList | Abstract Objective Recent work has bolstered the possibility that peripheral changes may be relevant to Alzheimer's disease pathogenesis in the brain. While age‐associated blood‐borne proteins have been targeted to restore function to the aged brain, it remains unclear whether other dysfunctional systemic states can be exploited for similar benefits. Here, we investigate whether APOE allelic variation or presence of brain amyloid are associated with plasma proteomic changes and the molecular processes associated with these changes. Methods Using the SOMAscan assay, we measured 1305 plasma proteins from 53 homozygous, APOE3 and APOE4 subjects without dementia. We investigated the relationship of either the APOE‐ε4 allele or amyloid positivity with plasma proteome changes by linear mixed effects modeling and ontology‐based pathway and module–trait correlation analyses. Results APOE4 is associated with plasma protein differences linked to atherosclerosis, tyrosine kinase activity, cholesterol transport, extracellular matrix, and synaptogenesis pathways. Independent of APOE4, we found that subjects likely harboring brain amyloid exhibit plasma proteome signatures associated with AD‐linked pathways, including neurovascular dysfunction. Interpretation Our results indicate that APOE4 status or presence of brain amyloid are associated with plasma proteomic shifts prior to the onset of symptoms, suggesting that systemic pathways in certain risk contexts may be plausible targets for disease modification. Recent work has bolstered the possibility that peripheral changes may be relevant to Alzheimer's disease pathogenesis in the brain. While age-associated blood-borne proteins have been targeted to restore function to the aged brain, it remains unclear whether other dysfunctional systemic states can be exploited for similar benefits. Here, we investigate whether APOE allelic variation or presence of brain amyloid are associated with plasma proteomic changes and the molecular processes associated with these changes.OBJECTIVERecent work has bolstered the possibility that peripheral changes may be relevant to Alzheimer's disease pathogenesis in the brain. While age-associated blood-borne proteins have been targeted to restore function to the aged brain, it remains unclear whether other dysfunctional systemic states can be exploited for similar benefits. Here, we investigate whether APOE allelic variation or presence of brain amyloid are associated with plasma proteomic changes and the molecular processes associated with these changes.Using the SOMAscan assay, we measured 1305 plasma proteins from 53 homozygous, APOE3 and APOE4 subjects without dementia. We investigated the relationship of either the APOE-ε4 allele or amyloid positivity with plasma proteome changes by linear mixed effects modeling and ontology-based pathway and module-trait correlation analyses.METHODSUsing the SOMAscan assay, we measured 1305 plasma proteins from 53 homozygous, APOE3 and APOE4 subjects without dementia. We investigated the relationship of either the APOE-ε4 allele or amyloid positivity with plasma proteome changes by linear mixed effects modeling and ontology-based pathway and module-trait correlation analyses.APOE4 is associated with plasma protein differences linked to atherosclerosis, tyrosine kinase activity, cholesterol transport, extracellular matrix, and synaptogenesis pathways. Independent of APOE4, we found that subjects likely harboring brain amyloid exhibit plasma proteome signatures associated with AD-linked pathways, including neurovascular dysfunction.RESULTSAPOE4 is associated with plasma protein differences linked to atherosclerosis, tyrosine kinase activity, cholesterol transport, extracellular matrix, and synaptogenesis pathways. Independent of APOE4, we found that subjects likely harboring brain amyloid exhibit plasma proteome signatures associated with AD-linked pathways, including neurovascular dysfunction.Our results indicate that APOE4 status or presence of brain amyloid are associated with plasma proteomic shifts prior to the onset of symptoms, suggesting that systemic pathways in certain risk contexts may be plausible targets for disease modification.INTERPRETATIONOur results indicate that APOE4 status or presence of brain amyloid are associated with plasma proteomic shifts prior to the onset of symptoms, suggesting that systemic pathways in certain risk contexts may be plausible targets for disease modification. Recent work has bolstered the possibility that peripheral changes may be relevant to Alzheimer's disease pathogenesis in the brain. While age-associated blood-borne proteins have been targeted to restore function to the aged brain, it remains unclear whether other dysfunctional systemic states can be exploited for similar benefits. Here, we investigate whether APOE allelic variation or presence of brain amyloid are associated with plasma proteomic changes and the molecular processes associated with these changes. Using the SOMAscan assay, we measured 1305 plasma proteins from 53 homozygous, APOE3 and APOE4 subjects without dementia. We investigated the relationship of either the APOE-ε4 allele or amyloid positivity with plasma proteome changes by linear mixed effects modeling and ontology-based pathway and module-trait correlation analyses. APOE4 is associated with plasma protein differences linked to atherosclerosis, tyrosine kinase activity, cholesterol transport, extracellular matrix, and synaptogenesis pathways. Independent of APOE4, we found that subjects likely harboring brain amyloid exhibit plasma proteome signatures associated with AD-linked pathways, including neurovascular dysfunction. Our results indicate that APOE4 status or presence of brain amyloid are associated with plasma proteomic shifts prior to the onset of symptoms, suggesting that systemic pathways in certain risk contexts may be plausible targets for disease modification. Objective Recent work has bolstered the possibility that peripheral changes may be relevant to Alzheimer's disease pathogenesis in the brain. While age‐associated blood‐borne proteins have been targeted to restore function to the aged brain, it remains unclear whether other dysfunctional systemic states can be exploited for similar benefits. Here, we investigate whether APOE allelic variation or presence of brain amyloid are associated with plasma proteomic changes and the molecular processes associated with these changes. Methods Using the SOMAscan assay, we measured 1305 plasma proteins from 53 homozygous, APOE3 and APOE4 subjects without dementia. We investigated the relationship of either the APOE‐ε4 allele or amyloid positivity with plasma proteome changes by linear mixed effects modeling and ontology‐based pathway and module–trait correlation analyses. Results APOE4 is associated with plasma protein differences linked to atherosclerosis, tyrosine kinase activity, cholesterol transport, extracellular matrix, and synaptogenesis pathways. Independent of APOE4, we found that subjects likely harboring brain amyloid exhibit plasma proteome signatures associated with AD‐linked pathways, including neurovascular dysfunction. Interpretation Our results indicate that APOE4 status or presence of brain amyloid are associated with plasma proteomic shifts prior to the onset of symptoms, suggesting that systemic pathways in certain risk contexts may be plausible targets for disease modification. Objective Recent work has bolstered the possibility that peripheral changes may be relevant to Alzheimer's disease pathogenesis in the brain. While age‐associated blood‐borne proteins have been targeted to restore function to the aged brain, it remains unclear whether other dysfunctional systemic states can be exploited for similar benefits. Here, we investigate whether APOE allelic variation or presence of brain amyloid are associated with plasma proteomic changes and the molecular processes associated with these changes. Methods Using the SOMAscan assay, we measured 1305 plasma proteins from 53 homozygous, APOE3 and APOE4 subjects without dementia. We investigated the relationship of either the APOE‐ε4 allele or amyloid positivity with plasma proteome changes by linear mixed effects modeling and ontology‐based pathway and module–trait correlation analyses. Results APOE4 is associated with plasma protein differences linked to atherosclerosis, tyrosine kinase activity, cholesterol transport, extracellular matrix, and synaptogenesis pathways. Independent of APOE4, we found that subjects likely harboring brain amyloid exhibit plasma proteome signatures associated with AD‐linked pathways, including neurovascular dysfunction. Interpretation Our results indicate that APOE4 status or presence of brain amyloid are associated with plasma proteomic shifts prior to the onset of symptoms, suggesting that systemic pathways in certain risk contexts may be plausible targets for disease modification. |
| Author | Castellano, Joseph M. Philippi, Sarah M. Raj, Towfique BP, Kailash |
| AuthorAffiliation | 2 Ronald M. Loeb Center for Alzheimer's Disease Icahn School of Medicine at Mount Sinai New York New York USA 3 Graduate School of Biomedical Sciences Icahn School of Medicine at Mount Sinai New York New York USA 5 Department of Genetics and Genomic Sciences, Icahn Institute for Data Science and Genomic Technology Icahn School of Medicine at Mount Sinai New York New York USA 4 Black Family Stem Cell Institute Icahn School of Medicine at Mount Sinai New York New York USA 1 Nash Family Department of Neuroscience, Department of Neurology, Friedman Brain Institute Icahn School of Medicine at Mount Sinai New York New York USA |
| AuthorAffiliation_xml | – name: 2 Ronald M. Loeb Center for Alzheimer's Disease Icahn School of Medicine at Mount Sinai New York New York USA – name: 4 Black Family Stem Cell Institute Icahn School of Medicine at Mount Sinai New York New York USA – name: 1 Nash Family Department of Neuroscience, Department of Neurology, Friedman Brain Institute Icahn School of Medicine at Mount Sinai New York New York USA – name: 5 Department of Genetics and Genomic Sciences, Icahn Institute for Data Science and Genomic Technology Icahn School of Medicine at Mount Sinai New York New York USA – name: 3 Graduate School of Biomedical Sciences Icahn School of Medicine at Mount Sinai New York New York USA |
| Author_xml | – sequence: 1 givenname: Sarah M. surname: Philippi fullname: Philippi, Sarah M. organization: Icahn School of Medicine at Mount Sinai – sequence: 2 givenname: Kailash surname: BP fullname: BP, Kailash organization: Icahn School of Medicine at Mount Sinai – sequence: 3 givenname: Towfique surname: Raj fullname: Raj, Towfique organization: Icahn School of Medicine at Mount Sinai – sequence: 4 givenname: Joseph M. orcidid: 0000-0002-8026-6292 surname: Castellano fullname: Castellano, Joseph M. email: joseph.castellano@mssm.edu organization: Icahn School of Medicine at Mount Sinai |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/39689057$$D View this record in MEDLINE/PubMed |
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| Snippet | Objective
Recent work has bolstered the possibility that peripheral changes may be relevant to Alzheimer's disease pathogenesis in the brain. While... Recent work has bolstered the possibility that peripheral changes may be relevant to Alzheimer's disease pathogenesis in the brain. While age-associated... Objective Recent work has bolstered the possibility that peripheral changes may be relevant to Alzheimer's disease pathogenesis in the brain. While... Abstract Objective Recent work has bolstered the possibility that peripheral changes may be relevant to Alzheimer's disease pathogenesis in the brain. While... |
| SourceID | doaj pubmedcentral proquest pubmed crossref wiley |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Publisher |
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| SubjectTerms | Age Aged Aged, 80 and over Aging Aging - genetics Alzheimer Disease - genetics Alzheimer's disease Apolipoprotein E4 - genetics Apolipoproteins E - genetics Brain - metabolism Brain research Cluster analysis Dementia Female Genotype Genotype & phenotype Health risk assessment Humans Male Ontology Plasma Proteins Proteome - metabolism Risk factors Sample variance Visualization |
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| Title | APOE genotype and brain amyloid are associated with changes in the plasma proteome in elderly subjects without dementia |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1002%2Facn3.52250 https://www.ncbi.nlm.nih.gov/pubmed/39689057 https://www.proquest.com/docview/3166110743 https://www.proquest.com/docview/3146943211 https://pubmed.ncbi.nlm.nih.gov/PMC11822792 https://doaj.org/article/9db859136a874849b67cc95db2f87367 |
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