Home > Publications Database > C1q is increased in cerebrospinal fluid-derived extracellular vesicles in Alzheimer's disease: A multi-cohort proteomics and immuno-assay validation study. > print

001     257583
005     20240826165950.0
024 7 _ |a 10.1002/alz.13066
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024 7 _ |a pmid:37023079
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024 7 _ |a 1552-5260
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024 7 _ |a 1552-5279
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024 7 _ |a altmetric:145204817
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037 _ _ |a DZNE-2023-00459
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Chatterjee, Madhurima
|0 P:(DE-2719)2812856
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|u dzne
245 _ _ |a C1q is increased in cerebrospinal fluid-derived extracellular vesicles in Alzheimer's disease: A multi-cohort proteomics and immuno-assay validation study.
260 _ _ |a Hoboken, NJ
|c 2023
|b Wiley
336 7 _ |a article
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336 7 _ |a ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a Extracellular vesicles (EVs) may propagate and modulate Alzheimer's disease (AD) pathology. We aimed to comprehensively characterize the proteome of cerebrospinal fluid (CSF) EVs to identify proteins and pathways altered in AD.CSF EVs were isolated by ultracentrifugation (Cohort 1) or Vn96 peptide (Cohort 2) from non-neurodegenerative controls (n = 15, 16) and AD patients (n = 22, 20, respectively). EVs were subjected to untargeted quantitative mass spectrometry-based proteomics. Results were validated by enzyme-linked immunosorbent assay (ELISA) in Cohorts 3 and 4, consisting of controls (n = 16, n = 43, (Cohort3, Cohort4)), and patients with AD (n = 24, n = 100).We found > 30 differentially expressed proteins in AD CSF EVs involved in immune-regulation. Increase of C1q levels in AD compared to non-demented controls was validated by ELISA (∼ 1.5 fold, p (Cohort 3) = 0.03, p (Cohort 4) = 0.005).EVs may be utilized as a potential biomarker and may play a so far unprecedented role in immune-regulation in AD.
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650 _ 7 |a Complement C1q
|0 80295-33-6
|2 NLM Chemicals
650 _ 7 |a Alzheimer's disease (AD)
|2 Other
650 _ 7 |a biomarker
|2 Other
650 _ 7 |a cerebrospinal fluid (CSF)
|2 Other
650 _ 7 |a complement
|2 Other
650 _ 7 |a extracellular vesicles
|2 Other
650 _ 7 |a immune system
|2 Other
650 _ 7 |a mild cognitive impairment (MCI)
|2 Other
650 _ 7 |a proteomics
|2 Other
650 _ 7 |a Amyloid beta-Peptides
|2 NLM Chemicals
650 _ 7 |a Peptide Fragments
|2 NLM Chemicals
650 _ 7 |a Biomarkers
|2 NLM Chemicals
650 _ 7 |a tau Proteins
|2 NLM Chemicals
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Alzheimer Disease: pathology
|2 MeSH
650 _ 2 |a Complement C1q
|2 MeSH
650 _ 2 |a Proteomics
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides: metabolism
|2 MeSH
650 _ 2 |a Peptide Fragments: cerebrospinal fluid
|2 MeSH
650 _ 2 |a Biomarkers: cerebrospinal fluid
|2 MeSH
650 _ 2 |a Extracellular Vesicles: metabolism
|2 MeSH
650 _ 2 |a tau Proteins: cerebrospinal fluid
|2 MeSH
650 _ 2 |a Cognitive Dysfunction: cerebrospinal fluid
|2 MeSH
700 1 _ |a Özdemir, Selcuk
|0 P:(DE-2719)9002048
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|u dzne
700 1 _ |a Kunadt, Marcel
|b 2
700 1 _ |a Koel-Simmelink, Marleen
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700 1 _ |a Boiten, Walter
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700 1 _ |a Piepkorn, Lars
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700 1 _ |a Pham, Thang V
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700 1 _ |a Chiasserini, Davide
|b 7
700 1 _ |a Piersma, Sander R
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700 1 _ |a Knol, Jaco C
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700 1 _ |a Möbius, Wiebke
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700 1 _ |a Mollenhauer, Brit
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700 1 _ |a van der Flier, Wiesje M
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700 1 _ |a Jimenez, Connie R
|b 13
700 1 _ |a Teunissen, Charlotte E
|b 14
700 1 _ |a Jahn, Olaf
|b 15
700 1 _ |a Schneider, Anja
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773 _ _ |a 10.1002/alz.13066
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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