Complement protein levels in plasma astrocyte‐derived exosomes are abnormal in conversion from mild cognitive impairment to Alzheimer's disease dementia
Abstract Introduction Levels of complement proteins (CPs) in plasma astrocyte‐derived exosomes (ADEs) that are abnormal in Alzheimer's disease (AD) have not been assessed in mild cognitive impairment (MCI). Methods Participants (n = 20 per group) had either MCI converting to dementia within 3 y...
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doaj-f4487646af6b4c2e880ba353df3a3c572020-11-25T03:02:58ZengWileyAlzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring2352-87292019-12-01111616610.1016/j.dadm.2018.11.002Complement protein levels in plasma astrocyte‐derived exosomes are abnormal in conversion from mild cognitive impairment to Alzheimer's disease dementiaCharisse N. Winston0Edward J. Goetzl1Janice B. Schwartz2Fanny M. Elahi3Robert A. Rissman4Department of NeurosciencesUniversity of CaliforniaSan DiegoLa JollaCAUSAJewish Home of San FranciscoSan FranciscoCAUSAJewish Home of San FranciscoSan FranciscoCAUSADepartment of NeurologyUniversity of CaliforniaSan FranciscoSan FranciscoCAUSADepartment of NeurosciencesUniversity of CaliforniaSan DiegoLa JollaCAUSAAbstract Introduction Levels of complement proteins (CPs) in plasma astrocyte‐derived exosomes (ADEs) that are abnormal in Alzheimer's disease (AD) have not been assessed in mild cognitive impairment (MCI). Methods Participants (n = 20 per group) had either MCI converting to dementia within 3 years (MCIC), MCI remaining stable over 3 years (MCIS), Alzheimer's disease, or were controls. CPs of ADEs isolated from plasmas by anti‐human glutamine aspartate transporter antibody absorption were quantified by ELISAs. Results ADE levels of C1q and C4b of the classical pathway, factor D and fragment Bb of the alternative pathway, and C5b, C3b, and C5b‐C9 of both pathways were significantly higher in patients with MCIC than those with MCIS. ADE levels of inhibitory CPs decay‐accelerating factor, CD46, CD59, and type 1 complement receptor were significantly lower in patients with MCIC than those with MCIS. Discussion ADE CPs are components of neurotoxic neuroinflammation that may be predictive biomarkers of MCI conversion to Alzheimer's disease.https://doi.org/10.1016/j.dadm.2018.11.002NeuroinflammationNeurodegenerationBiomarkersCognitive lossComplement regulators |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Charisse N. Winston Edward J. Goetzl Janice B. Schwartz Fanny M. Elahi Robert A. Rissman |
spellingShingle |
Charisse N. Winston Edward J. Goetzl Janice B. Schwartz Fanny M. Elahi Robert A. Rissman Complement protein levels in plasma astrocyte‐derived exosomes are abnormal in conversion from mild cognitive impairment to Alzheimer's disease dementia Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring Neuroinflammation Neurodegeneration Biomarkers Cognitive loss Complement regulators |
author_facet |
Charisse N. Winston Edward J. Goetzl Janice B. Schwartz Fanny M. Elahi Robert A. Rissman |
author_sort |
Charisse N. Winston |
title |
Complement protein levels in plasma astrocyte‐derived exosomes are abnormal in conversion from mild cognitive impairment to Alzheimer's disease dementia |
title_short |
Complement protein levels in plasma astrocyte‐derived exosomes are abnormal in conversion from mild cognitive impairment to Alzheimer's disease dementia |
title_full |
Complement protein levels in plasma astrocyte‐derived exosomes are abnormal in conversion from mild cognitive impairment to Alzheimer's disease dementia |
title_fullStr |
Complement protein levels in plasma astrocyte‐derived exosomes are abnormal in conversion from mild cognitive impairment to Alzheimer's disease dementia |
title_full_unstemmed |
Complement protein levels in plasma astrocyte‐derived exosomes are abnormal in conversion from mild cognitive impairment to Alzheimer's disease dementia |
title_sort |
complement protein levels in plasma astrocyte‐derived exosomes are abnormal in conversion from mild cognitive impairment to alzheimer's disease dementia |
publisher |
Wiley |
series |
Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring |
issn |
2352-8729 |
publishDate |
2019-12-01 |
description |
Abstract Introduction Levels of complement proteins (CPs) in plasma astrocyte‐derived exosomes (ADEs) that are abnormal in Alzheimer's disease (AD) have not been assessed in mild cognitive impairment (MCI). Methods Participants (n = 20 per group) had either MCI converting to dementia within 3 years (MCIC), MCI remaining stable over 3 years (MCIS), Alzheimer's disease, or were controls. CPs of ADEs isolated from plasmas by anti‐human glutamine aspartate transporter antibody absorption were quantified by ELISAs. Results ADE levels of C1q and C4b of the classical pathway, factor D and fragment Bb of the alternative pathway, and C5b, C3b, and C5b‐C9 of both pathways were significantly higher in patients with MCIC than those with MCIS. ADE levels of inhibitory CPs decay‐accelerating factor, CD46, CD59, and type 1 complement receptor were significantly lower in patients with MCIC than those with MCIS. Discussion ADE CPs are components of neurotoxic neuroinflammation that may be predictive biomarkers of MCI conversion to Alzheimer's disease. |
topic |
Neuroinflammation Neurodegeneration Biomarkers Cognitive loss Complement regulators |
url |
https://doi.org/10.1016/j.dadm.2018.11.002 |
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