α‐Synuclein Seed Amplification in CSF and Brain from Patients with Different Brain Distributions of Pathological α‐Synuclein in the Context of Co‐Pathology and Non‐LBD Diagnoses
Objective The purpose of this study was to determine the sensitivity and specificity of α‐synuclein seed amplification assay (αSyn‐SAA) in antemortem and postmortem cerebrospinal fluid (CSF) of autopsy‐confirmed patients with different distributions of pathological αSyn, co‐pathologies, and clinical...
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| Published in | Annals of neurology Vol. 92; no. 4; pp. 650 - 662 |
|---|---|
| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hoboken, USA
John Wiley & Sons, Inc
01.10.2022
Wiley Subscription Services, Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0364-5134 1531-8249 1531-8249 |
| DOI | 10.1002/ana.26453 |
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| Abstract | Objective
The purpose of this study was to determine the sensitivity and specificity of α‐synuclein seed amplification assay (αSyn‐SAA) in antemortem and postmortem cerebrospinal fluid (CSF) of autopsy‐confirmed patients with different distributions of pathological αSyn, co‐pathologies, and clinical diagnoses.
Methods
The αSyn‐SAA was used to test antemortem CSF samples from 119 subjects with a variety of clinical syndromes and standardized neuropathological examinations from Oregon Health and Science University (OHSU) and University of California San Diego (UCSD; 56 additional postmortem CSF samples available). The αSyn‐SAA was also applied to frontal cortex and amygdala homogenates. Sensitivity and specificity were compared across distributions of αSyn pathology. Clinical data and co‐pathologies were compared across αSyn‐SAA positive and negative groups.
Results
Fifty‐three individuals without and 66 with αSyn‐pathology (neocortical [n = 38], limbic [n = 7], and amygdala‐predominant [n = 21]) were included. There was a sensitivity of 97.8% and specificity of 98.1% of the αSyn‐SAA to identify patients with limbic/neocortical pathology from antemortem CSF. Sensitivity to detect amygdala‐predominant pathology was only 14.3%. Postmortem CSF and brain tissue αSyn‐SAA analyses also showed higher assay positivity in samples from limbic/neocortical cases.
Interpretation
CSF αSyn‐SAA reliably identifies αSyn seeds in patients with diffuse αSyn pathology in the context of co‐pathology and non‐Lewy body disease (LBD) diagnoses. The analysis of brain homogenates suggests that pathological αSyn in the amygdala might differ from pathological αSyn in the frontal cortex. The αSyn‐SAA might facilitate the differential diagnosis of dementias with mixed pathologies. ANN NEUROL 2022;92:650–662 |
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| AbstractList | The purpose of this study was to determine the sensitivity and specificity of α-synuclein seed amplification assay (αSyn-SAA) in antemortem and postmortem cerebrospinal fluid (CSF) of autopsy-confirmed patients with different distributions of pathological αSyn, co-pathologies, and clinical diagnoses.
The αSyn-SAA was used to test antemortem CSF samples from 119 subjects with a variety of clinical syndromes and standardized neuropathological examinations from Oregon Health and Science University (OHSU) and University of California San Diego (UCSD; 56 additional postmortem CSF samples available). The αSyn-SAA was also applied to frontal cortex and amygdala homogenates. Sensitivity and specificity were compared across distributions of αSyn pathology. Clinical data and co-pathologies were compared across αSyn-SAA positive and negative groups.
Fifty-three individuals without and 66 with αSyn-pathology (neocortical [n = 38], limbic [n = 7], and amygdala-predominant [n = 21]) were included. There was a sensitivity of 97.8% and specificity of 98.1% of the αSyn-SAA to identify patients with limbic/neocortical pathology from antemortem CSF. Sensitivity to detect amygdala-predominant pathology was only 14.3%. Postmortem CSF and brain tissue αSyn-SAA analyses also showed higher assay positivity in samples from limbic/neocortical cases.
CSF αSyn-SAA reliably identifies αSyn seeds in patients with diffuse αSyn pathology in the context of co-pathology and non-Lewy body disease (LBD) diagnoses. The analysis of brain homogenates suggests that pathological αSyn in the amygdala might differ from pathological αSyn in the frontal cortex. The αSyn-SAA might facilitate the differential diagnosis of dementias with mixed pathologies. ANN NEUROL 2022;92:650-662. The purpose of this study was to determine the sensitivity and specificity of α-synuclein seed amplification assay (αSyn-SAA) in antemortem and postmortem cerebrospinal fluid (CSF) of autopsy-confirmed patients with different distributions of pathological αSyn, co-pathologies, and clinical diagnoses.OBJECTIVEThe purpose of this study was to determine the sensitivity and specificity of α-synuclein seed amplification assay (αSyn-SAA) in antemortem and postmortem cerebrospinal fluid (CSF) of autopsy-confirmed patients with different distributions of pathological αSyn, co-pathologies, and clinical diagnoses.The αSyn-SAA was used to test antemortem CSF samples from 119 subjects with a variety of clinical syndromes and standardized neuropathological examinations from Oregon Health and Science University (OHSU) and University of California San Diego (UCSD; 56 additional postmortem CSF samples available). The αSyn-SAA was also applied to frontal cortex and amygdala homogenates. Sensitivity and specificity were compared across distributions of αSyn pathology. Clinical data and co-pathologies were compared across αSyn-SAA positive and negative groups.METHODSThe αSyn-SAA was used to test antemortem CSF samples from 119 subjects with a variety of clinical syndromes and standardized neuropathological examinations from Oregon Health and Science University (OHSU) and University of California San Diego (UCSD; 56 additional postmortem CSF samples available). The αSyn-SAA was also applied to frontal cortex and amygdala homogenates. Sensitivity and specificity were compared across distributions of αSyn pathology. Clinical data and co-pathologies were compared across αSyn-SAA positive and negative groups.Fifty-three individuals without and 66 with αSyn-pathology (neocortical [n = 38], limbic [n = 7], and amygdala-predominant [n = 21]) were included. There was a sensitivity of 97.8% and specificity of 98.1% of the αSyn-SAA to identify patients with limbic/neocortical pathology from antemortem CSF. Sensitivity to detect amygdala-predominant pathology was only 14.3%. Postmortem CSF and brain tissue αSyn-SAA analyses also showed higher assay positivity in samples from limbic/neocortical cases.RESULTSFifty-three individuals without and 66 with αSyn-pathology (neocortical [n = 38], limbic [n = 7], and amygdala-predominant [n = 21]) were included. There was a sensitivity of 97.8% and specificity of 98.1% of the αSyn-SAA to identify patients with limbic/neocortical pathology from antemortem CSF. Sensitivity to detect amygdala-predominant pathology was only 14.3%. Postmortem CSF and brain tissue αSyn-SAA analyses also showed higher assay positivity in samples from limbic/neocortical cases.CSF αSyn-SAA reliably identifies αSyn seeds in patients with diffuse αSyn pathology in the context of co-pathology and non-Lewy body disease (LBD) diagnoses. The analysis of brain homogenates suggests that pathological αSyn in the amygdala might differ from pathological αSyn in the frontal cortex. The αSyn-SAA might facilitate the differential diagnosis of dementias with mixed pathologies. ANN NEUROL 2022;92:650-662.INTERPRETATIONCSF αSyn-SAA reliably identifies αSyn seeds in patients with diffuse αSyn pathology in the context of co-pathology and non-Lewy body disease (LBD) diagnoses. The analysis of brain homogenates suggests that pathological αSyn in the amygdala might differ from pathological αSyn in the frontal cortex. The αSyn-SAA might facilitate the differential diagnosis of dementias with mixed pathologies. ANN NEUROL 2022;92:650-662. Objective The purpose of this study was to determine the sensitivity and specificity of α‐synuclein seed amplification assay (αSyn‐SAA) in antemortem and postmortem cerebrospinal fluid (CSF) of autopsy‐confirmed patients with different distributions of pathological αSyn, co‐pathologies, and clinical diagnoses. Methods The αSyn‐SAA was used to test antemortem CSF samples from 119 subjects with a variety of clinical syndromes and standardized neuropathological examinations from Oregon Health and Science University (OHSU) and University of California San Diego (UCSD; 56 additional postmortem CSF samples available). The αSyn‐SAA was also applied to frontal cortex and amygdala homogenates. Sensitivity and specificity were compared across distributions of αSyn pathology. Clinical data and co‐pathologies were compared across αSyn‐SAA positive and negative groups. Results Fifty‐three individuals without and 66 with αSyn‐pathology (neocortical [n = 38], limbic [n = 7], and amygdala‐predominant [n = 21]) were included. There was a sensitivity of 97.8% and specificity of 98.1% of the αSyn‐SAA to identify patients with limbic/neocortical pathology from antemortem CSF. Sensitivity to detect amygdala‐predominant pathology was only 14.3%. Postmortem CSF and brain tissue αSyn‐SAA analyses also showed higher assay positivity in samples from limbic/neocortical cases. Interpretation CSF αSyn‐SAA reliably identifies αSyn seeds in patients with diffuse αSyn pathology in the context of co‐pathology and non‐Lewy body disease (LBD) diagnoses. The analysis of brain homogenates suggests that pathological αSyn in the amygdala might differ from pathological αSyn in the frontal cortex. The αSyn‐SAA might facilitate the differential diagnosis of dementias with mixed pathologies. ANN NEUROL 2022;92:650–662 ObjectiveThe purpose of this study was to determine the sensitivity and specificity of α‐synuclein seed amplification assay (αSyn‐SAA) in antemortem and postmortem cerebrospinal fluid (CSF) of autopsy‐confirmed patients with different distributions of pathological αSyn, co‐pathologies, and clinical diagnoses.MethodsThe αSyn‐SAA was used to test antemortem CSF samples from 119 subjects with a variety of clinical syndromes and standardized neuropathological examinations from Oregon Health and Science University (OHSU) and University of California San Diego (UCSD; 56 additional postmortem CSF samples available). The αSyn‐SAA was also applied to frontal cortex and amygdala homogenates. Sensitivity and specificity were compared across distributions of αSyn pathology. Clinical data and co‐pathologies were compared across αSyn‐SAA positive and negative groups.ResultsFifty‐three individuals without and 66 with αSyn‐pathology (neocortical [n = 38], limbic [n = 7], and amygdala‐predominant [n = 21]) were included. There was a sensitivity of 97.8% and specificity of 98.1% of the αSyn‐SAA to identify patients with limbic/neocortical pathology from antemortem CSF. Sensitivity to detect amygdala‐predominant pathology was only 14.3%. Postmortem CSF and brain tissue αSyn‐SAA analyses also showed higher assay positivity in samples from limbic/neocortical cases.InterpretationCSF αSyn‐SAA reliably identifies αSyn seeds in patients with diffuse αSyn pathology in the context of co‐pathology and non‐Lewy body disease (LBD) diagnoses. The analysis of brain homogenates suggests that pathological αSyn in the amygdala might differ from pathological αSyn in the frontal cortex. The αSyn‐SAA might facilitate the differential diagnosis of dementias with mixed pathologies. ANN NEUROL 2022;92:650–662 |
| Author | Hiniker, Annie Concha‐Marambio, Luis Galasko, Doug R. Woltjer, Randy L. Quinn, Joseph F. Ma, Yihua Wilson, Edward N. Brumbach, Barbara H. Kim, Yongya Smirnov, Denis S. Kaye, Jeffrey A. Coughlin, David G. Arnold, Moriah R. Farris, Carly M. |
| AuthorAffiliation | 2 Department of Neurosciences, University of California San Diego 7 Department of Pathology, University of California San Diego 5 Department of Neurology & Neurological Sciences, Stanford University 3 Biostatistics and Design Program, Oregon Health and Science University 8 Department of Pathology, Oregon Health and Science University 1 Medical Scientist Training Program, Oregon Health and Science University 4 Amprion Inc 6 Department of Neurology, Oregon Health and Science University 9 Portland VA Medical Center, Parkinson’s Disease Research Education and Clinical Care Center (PADRECC) |
| AuthorAffiliation_xml | – name: 7 Department of Pathology, University of California San Diego – name: 2 Department of Neurosciences, University of California San Diego – name: 9 Portland VA Medical Center, Parkinson’s Disease Research Education and Clinical Care Center (PADRECC) – name: 3 Biostatistics and Design Program, Oregon Health and Science University – name: 8 Department of Pathology, Oregon Health and Science University – name: 1 Medical Scientist Training Program, Oregon Health and Science University – name: 4 Amprion Inc – name: 6 Department of Neurology, Oregon Health and Science University – name: 5 Department of Neurology & Neurological Sciences, Stanford University |
| Author_xml | – sequence: 1 givenname: Moriah R. orcidid: 0000-0002-5916-7978 surname: Arnold fullname: Arnold, Moriah R. organization: Oregon Health and Science University – sequence: 2 givenname: David G. surname: Coughlin fullname: Coughlin, David G. organization: University of California San Diego – sequence: 3 givenname: Barbara H. surname: Brumbach fullname: Brumbach, Barbara H. organization: Oregon Health and Science University – sequence: 4 givenname: Denis S. orcidid: 0000-0002-9768-313X surname: Smirnov fullname: Smirnov, Denis S. organization: University of California San Diego – sequence: 5 givenname: Luis orcidid: 0000-0002-9454-8389 surname: Concha‐Marambio fullname: Concha‐Marambio, Luis organization: Amprion Inc – sequence: 6 givenname: Carly M. orcidid: 0000-0002-8277-8531 surname: Farris fullname: Farris, Carly M. organization: Amprion Inc – sequence: 7 givenname: Yihua surname: Ma fullname: Ma, Yihua organization: Amprion Inc – sequence: 8 givenname: Yongya orcidid: 0000-0002-4501-3660 surname: Kim fullname: Kim, Yongya organization: University of California San Diego – sequence: 9 givenname: Edward N. orcidid: 0000-0003-0640-5247 surname: Wilson fullname: Wilson, Edward N. organization: Stanford University – sequence: 10 givenname: Jeffrey A. orcidid: 0000-0002-9971-3478 surname: Kaye fullname: Kaye, Jeffrey A. organization: Oregon Health and Science University – sequence: 11 givenname: Annie orcidid: 0000-0002-0055-6610 surname: Hiniker fullname: Hiniker, Annie organization: University of California San Diego – sequence: 12 givenname: Randy L. surname: Woltjer fullname: Woltjer, Randy L. organization: Oregon Health and Science University – sequence: 13 givenname: Doug R. orcidid: 0000-0001-6195-3241 surname: Galasko fullname: Galasko, Doug R. organization: University of California San Diego – sequence: 14 givenname: Joseph F. surname: Quinn fullname: Quinn, Joseph F. email: quinnj@ohsu.edu organization: Portland Virginia Medical Center, Parkinson's Disease Research Education and Clinical Care Center (PADRECC) |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35808984$$D View this record in MEDLINE/PubMed |
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| Notes | Moriah R. Arnold and David G. Coughlin contributed equally to this work. Correction added on Aug 5, 2022, after first online publication: Author contribution text is revised. ORCID ids were added for the authors. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 MRA, DGC, DSS, LCM, DRG, and JFQ contributed to the conception and design of the study; MRA, DGC, BHB, DSS, LCM, CMF, YM, YK, ENW, JAK, AH, and RLW contributed to the acquisition and analysis of data; MRA, DGC, BHB, LCM, DRG, and JFQ contributed to drafting the text or preparing the figures. authors contributed equally Author Contributions |
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The purpose of this study was to determine the sensitivity and specificity of α‐synuclein seed amplification assay (αSyn‐SAA) in antemortem and... The purpose of this study was to determine the sensitivity and specificity of α-synuclein seed amplification assay (αSyn-SAA) in antemortem and postmortem... ObjectiveThe purpose of this study was to determine the sensitivity and specificity of α‐synuclein seed amplification assay (αSyn‐SAA) in antemortem and... |
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| SubjectTerms | alpha-Synuclein - metabolism Amplification Amygdala Autopsies Autopsy Brain Brain - pathology Cerebrospinal fluid Cortex (frontal) Differential diagnosis Humans Lewy bodies Lewy body disease Pathology Patients Seeds Sensitivity Sensitivity and Specificity Synuclein Tissue analysis |
| Title | α‐Synuclein Seed Amplification in CSF and Brain from Patients with Different Brain Distributions of Pathological α‐Synuclein in the Context of Co‐Pathology and Non‐LBD Diagnoses |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fana.26453 https://www.ncbi.nlm.nih.gov/pubmed/35808984 https://www.proquest.com/docview/2715399201 https://www.proquest.com/docview/2687724028 https://pubmed.ncbi.nlm.nih.gov/PMC9489647 |
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