2018
DOI: 10.1002/ana.25172
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High complement levels in astrocyte‐derived exosomes of Alzheimer disease

Abstract: ADE complement effector proteins in AD are produced by dysregulated systems, attain higher levels than in controls, and may potentially damage neurons in the late inflammatory phase of AD. Ann Neurol 2018;83:544-552.

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Cited by 288 publications
(295 citation statements)
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“…A1 astrocytes lose most of their original astrocyte function and exhibit new functions where they secrete toxins that induce apoptosis of neurons and are toxic to synapses and the myelin sheath. C3 is a marker for A1 astrocytes but not expressed in A2 astrocytes [6,35,37,40]. In this study, C3/GFAP was used as a double-marker for labeling A1 reactive astrocytes in the spinal cord.…”
Section: Discussionmentioning
confidence: 98%
“…A1 astrocytes lose most of their original astrocyte function and exhibit new functions where they secrete toxins that induce apoptosis of neurons and are toxic to synapses and the myelin sheath. C3 is a marker for A1 astrocytes but not expressed in A2 astrocytes [6,35,37,40]. In this study, C3/GFAP was used as a double-marker for labeling A1 reactive astrocytes in the spinal cord.…”
Section: Discussionmentioning
confidence: 98%
“…Chronically activated disease‐associated microglia are present in the CNS tissue of patients with various neurodegenerative diseases, including AD, and they release pro‐inflammatory cytokines, particularly IL‐1α, TNF‐α, and C1q, which lead to downstream activation of astrocytes (Liddelow et al, ). Disease‐associated “A1” astrocytes express various complements including C1q, C1r, C1s, C3, and C4 (Stephan, Barres, & Stevens, ; Stevens et al, ) and down‐regulate various complement regulatory proteins such as CD59, CD46, DAF, and CR1 (Goetzl, Schwartz, Abner, Jicha, & Kapogiannis, ). “A1” astrocytes have been identified in several neurodegenerative diseases including AD, Huntington's disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis.…”
Section: Complementmentioning
confidence: 99%
“…Glia also represent a relatively novel and untapped source of biomarkers for neurodegenerative diseases. In AD patients, peripherally circulating astrocyte‐derived exosomes (ADEs) extracted from blood plasma contain increased levels of complement proteins . Because C3 complement protein is a key marker of A1 astrocytes (which are elevated in AD tissue), these data suggest that ADEs could encapsulate an accessible measure of astrocyte reactivity.…”
Section: Bringing Glia Into Focus In Pd Researchmentioning
confidence: 99%