Complement protein levels in plasma astrocyte-derived exosomes are abnormal in conversion from mild cognitive impairment to Alzheimer's disease dementia

Charisse N. Winston; Edward J. Goetzl; Janice B. Schwartz; Fanny M. Elahi; Robert A. Rissman

doi:10.1016/j.dadm.2018.11.002

Complement protein levels in plasma astrocyte-derived exosomes are abnormal in conversion from mild cognitive impairment to Alzheimer's disease dementia

Charisse N. Winston, Edward J. Goetzl, Janice B. Schwartz, Fanny M. Elahi, Robert A. Rissman

Research output: Contribution to journal › Article › peer-review

89 Scopus citations

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.

Original language	English
Pages (from-to)	61-66
Number of pages	6
Journal	Alzheimer's and Dementia: Diagnosis, Assessment and Disease Monitoring
Volume	11
DOIs	https://doi.org/10.1016/j.dadm.2018.11.002
State	Published - Dec 2019
Externally published	Yes

Keywords

Biomarkers
Cognitive loss
Complement regulators
Neurodegeneration
Neuroinflammation

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10.1016/j.dadm.2018.11.002

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title = "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 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.",

keywords = "Biomarkers, Cognitive loss, Complement regulators, Neurodegeneration, Neuroinflammation",

author = "Winston, {Charisse N.} and Goetzl, {Edward J.} and Schwartz, {Janice B.} and Elahi, {Fanny M.} and Rissman, {Robert A.}",

note = "Publisher Copyright: {\textcopyright} 2018 The Authors",

year = "2019",

month = dec,

doi = "10.1016/j.dadm.2018.11.002",

language = "English",

volume = "11",

pages = "61--66",

journal = "Alzheimer's and Dementia: Diagnosis, Assessment and Disease Monitoring",

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Complement protein levels in plasma astrocyte-derived exosomes are abnormal in conversion from mild cognitive impairment to Alzheimer's disease dementia. / Winston, Charisse N.; Goetzl, Edward J.; Schwartz, Janice B. et al.
In: Alzheimer's and Dementia: Diagnosis, Assessment and Disease Monitoring, Vol. 11, 12.2019, p. 61-66.

Research output: Contribution to journal › Article › peer-review

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AU - Winston, Charisse N.

AU - Goetzl, Edward J.

AU - Schwartz, Janice B.

AU - Elahi, Fanny M.

AU - Rissman, Robert A.

PY - 2019/12

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AB - 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.

KW - Biomarkers

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ER -

Complement protein levels in plasma astrocyte-derived exosomes are abnormal in conversion from mild cognitive impairment to Alzheimer's disease dementia

Abstract

Keywords

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