Clinical performance and head-to-head comparison of CSF p-tau235 with p-tau181, p-tau217 and p-tau231 in two memory clinic cohorts

Abstract Background Cerebrospinal fluid (CSF) p-tau235 is a novel biomarker highly specific of Alzheimer’s disease (AD). However, CSF p-tau235 has only been studied in well-characterized research cohorts, which do not fully reflect the patient landscape found in clinical settings. Therefore, in this multicentre study, we investigated the performance of CSF p-tau235 to detect symptomatic AD in clinical settings and compared it with CSF p-tau181, p-tau217 and p-tau231. Methods CSF p-tau235 was measured using an in-house single molecule array (Simoa) assay in two independent memory clinic cohorts: Paris cohort (Lariboisière Fernand-Widal University Hospital Paris, France; n=212) and BIODEGMAR cohort (Hospital del Mar, Barcelona, Spain; n=175). Patients were classified by the syndromic diagnosis (cognitively unimpaired [CU], mild cognitive impairment [MCI] or dementia) and their biological diagnosis (amyloid-beta [Aβ]+ or Aβ $$-$$ - ). Both cohorts included detailed cognitive assessments and CSF biomarker measurements (clinically validated core AD biomarkers [Lumipulse CSF Aβ1–42/40 ratio, p-tau181 and t-tau] and in-house developed Simoa CSF p-tau181, p-tau217 and p-tau231). Results High CSF p-tau235 levels were strongly associated with CSF amyloidosis regardless of the clinical diagnosis, being significantly increased in MCI Aβ+ and dementia Aβ+ when compared with all other Aβ− groups (Paris cohort: P ˂0.0001 for all; BIODEGMAR cohort: P ˂0.05 for all). CSF p-tau235 was pronouncedly increased in the A+T+ profile group compared with A−T− and A+T− groups (P ˂0.0001 for all). Moreover, CSF p-tau235 demonstrated high diagnostic accuracies identifying CSF amyloidosis in symptomatic cases (AUCs=0.86 to 0.96) and discriminating AT groups (AUCs=0.79 to 0.98). Overall, CSF p-tau235 showed similar performances to CSF p-tau181 and CSF p-tau231 when discriminating CSF amyloidosis in various scenarios, but lower than CSF p-tau217. Finally, CSF p-tau235 associated with global cognition and memory domain in both cohorts. Conclusions CSF p-tau235 was increased with the presence of CSF amyloidosis in two independent memory clinic cohorts. CSF p-tau235 accurately identified AD in both MCI and dementia patients. Overall, the diagnostic performance of CSF p-tau235 was comparable to that of other CSF p-tau measurements, indicating its suitability to support a biomarker-based AD diagnosis in clinical settings. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Juan Lantero-Rodriguez [verfasserIn] Agathe Vrillon [verfasserIn] Aida Fernández-Lebrero [verfasserIn] Paula Ortiz-Romero [verfasserIn] Anniina Snellman [verfasserIn] Laia Montoliu-Gaya [verfasserIn] Wagner S. Brum [verfasserIn] Emmanuel Cognat [verfasserIn] Julien Dumurgier [verfasserIn] Albert Puig-Pijoan [verfasserIn] Irene Navalpotro-Gómez [verfasserIn] Greta García-Escobar [verfasserIn] Thomas K. Karikari [verfasserIn] Eugeen Vanmechelen [verfasserIn] Nicholas J. Ashton [verfasserIn] Henrik Zetterberg [verfasserIn] Marc Suárez-Calvet [verfasserIn] Claire Paquet [verfasserIn] Kaj Blennow [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	Alzheimer’s disease CSF Biomarkers p-tau235 p-tau181 p-tau217

Übergeordnetes Werk:	In: Alzheimer’s Research & Therapy - BMC, 2015, 15(2023), 1, Seite 15
Übergeordnetes Werk:	volume:15 ; year:2023 ; number:1 ; pages:15

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/s13195-023-01201-0

Katalog-ID:	DOAJ087766833

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100	0		\|a Juan Lantero-Rodriguez \|e verfasserin \|4 aut
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520			\|a Abstract Background Cerebrospinal fluid (CSF) p-tau235 is a novel biomarker highly specific of Alzheimer’s disease (AD). However, CSF p-tau235 has only been studied in well-characterized research cohorts, which do not fully reflect the patient landscape found in clinical settings. Therefore, in this multicentre study, we investigated the performance of CSF p-tau235 to detect symptomatic AD in clinical settings and compared it with CSF p-tau181, p-tau217 and p-tau231. Methods CSF p-tau235 was measured using an in-house single molecule array (Simoa) assay in two independent memory clinic cohorts: Paris cohort (Lariboisière Fernand-Widal University Hospital Paris, France; n=212) and BIODEGMAR cohort (Hospital del Mar, Barcelona, Spain; n=175). Patients were classified by the syndromic diagnosis (cognitively unimpaired [CU], mild cognitive impairment [MCI] or dementia) and their biological diagnosis (amyloid-beta [Aβ]+ or Aβ $$-$$ - ). Both cohorts included detailed cognitive assessments and CSF biomarker measurements (clinically validated core AD biomarkers [Lumipulse CSF Aβ1–42/40 ratio, p-tau181 and t-tau] and in-house developed Simoa CSF p-tau181, p-tau217 and p-tau231). Results High CSF p-tau235 levels were strongly associated with CSF amyloidosis regardless of the clinical diagnosis, being significantly increased in MCI Aβ+ and dementia Aβ+ when compared with all other Aβ− groups (Paris cohort: P ˂0.0001 for all; BIODEGMAR cohort: P ˂0.05 for all). CSF p-tau235 was pronouncedly increased in the A+T+ profile group compared with A−T− and A+T− groups (P ˂0.0001 for all). Moreover, CSF p-tau235 demonstrated high diagnostic accuracies identifying CSF amyloidosis in symptomatic cases (AUCs=0.86 to 0.96) and discriminating AT groups (AUCs=0.79 to 0.98). Overall, CSF p-tau235 showed similar performances to CSF p-tau181 and CSF p-tau231 when discriminating CSF amyloidosis in various scenarios, but lower than CSF p-tau217. Finally, CSF p-tau235 associated with global cognition and memory domain in both cohorts. Conclusions CSF p-tau235 was increased with the presence of CSF amyloidosis in two independent memory clinic cohorts. CSF p-tau235 accurately identified AD in both MCI and dementia patients. Overall, the diagnostic performance of CSF p-tau235 was comparable to that of other CSF p-tau measurements, indicating its suitability to support a biomarker-based AD diagnosis in clinical settings.
650		4	\|a Alzheimer’s disease
650		4	\|a CSF
650		4	\|a Biomarkers
650		4	\|a p-tau235
650		4	\|a p-tau181
650		4	\|a p-tau217
653		0	\|a Neurosciences. Biological psychiatry. Neuropsychiatry
653		0	\|a Neurology. Diseases of the nervous system
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700	0		\|a Aida Fernández-Lebrero \|e verfasserin \|4 aut
700	0		\|a Paula Ortiz-Romero \|e verfasserin \|4 aut
700	0		\|a Anniina Snellman \|e verfasserin \|4 aut
700	0		\|a Laia Montoliu-Gaya \|e verfasserin \|4 aut
700	0		\|a Wagner S. Brum \|e verfasserin \|4 aut
700	0		\|a Emmanuel Cognat \|e verfasserin \|4 aut
700	0		\|a Julien Dumurgier \|e verfasserin \|4 aut
700	0		\|a Albert Puig-Pijoan \|e verfasserin \|4 aut
700	0		\|a Irene Navalpotro-Gómez \|e verfasserin \|4 aut
700	0		\|a Greta García-Escobar \|e verfasserin \|4 aut
700	0		\|a Thomas K. Karikari \|e verfasserin \|4 aut
700	0		\|a Eugeen Vanmechelen \|e verfasserin \|4 aut
700	0		\|a Nicholas J. Ashton \|e verfasserin \|4 aut
700	0		\|a Henrik Zetterberg \|e verfasserin \|4 aut
700	0		\|a Marc Suárez-Calvet \|e verfasserin \|4 aut
700	0		\|a Claire Paquet \|e verfasserin \|4 aut
700	0		\|a Kaj Blennow \|e verfasserin \|4 aut
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allfields	10.1186/s13195-023-01201-0 doi (DE-627)DOAJ087766833 (DE-599)DOAJ77904aa0f595409998732159a64f7f99 DE-627 ger DE-627 rakwb eng RC321-571 RC346-429 Juan Lantero-Rodriguez verfasserin aut Clinical performance and head-to-head comparison of CSF p-tau235 with p-tau181, p-tau217 and p-tau231 in two memory clinic cohorts 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Cerebrospinal fluid (CSF) p-tau235 is a novel biomarker highly specific of Alzheimer’s disease (AD). However, CSF p-tau235 has only been studied in well-characterized research cohorts, which do not fully reflect the patient landscape found in clinical settings. Therefore, in this multicentre study, we investigated the performance of CSF p-tau235 to detect symptomatic AD in clinical settings and compared it with CSF p-tau181, p-tau217 and p-tau231. Methods CSF p-tau235 was measured using an in-house single molecule array (Simoa) assay in two independent memory clinic cohorts: Paris cohort (Lariboisière Fernand-Widal University Hospital Paris, France; n=212) and BIODEGMAR cohort (Hospital del Mar, Barcelona, Spain; n=175). Patients were classified by the syndromic diagnosis (cognitively unimpaired [CU], mild cognitive impairment [MCI] or dementia) and their biological diagnosis (amyloid-beta [Aβ]+ or Aβ $$-$$ - ). Both cohorts included detailed cognitive assessments and CSF biomarker measurements (clinically validated core AD biomarkers [Lumipulse CSF Aβ1–42/40 ratio, p-tau181 and t-tau] and in-house developed Simoa CSF p-tau181, p-tau217 and p-tau231). Results High CSF p-tau235 levels were strongly associated with CSF amyloidosis regardless of the clinical diagnosis, being significantly increased in MCI Aβ+ and dementia Aβ+ when compared with all other Aβ− groups (Paris cohort: P ˂0.0001 for all; BIODEGMAR cohort: P ˂0.05 for all). CSF p-tau235 was pronouncedly increased in the A+T+ profile group compared with A−T− and A+T− groups (P ˂0.0001 for all). Moreover, CSF p-tau235 demonstrated high diagnostic accuracies identifying CSF amyloidosis in symptomatic cases (AUCs=0.86 to 0.96) and discriminating AT groups (AUCs=0.79 to 0.98). Overall, CSF p-tau235 showed similar performances to CSF p-tau181 and CSF p-tau231 when discriminating CSF amyloidosis in various scenarios, but lower than CSF p-tau217. Finally, CSF p-tau235 associated with global cognition and memory domain in both cohorts. Conclusions CSF p-tau235 was increased with the presence of CSF amyloidosis in two independent memory clinic cohorts. CSF p-tau235 accurately identified AD in both MCI and dementia patients. Overall, the diagnostic performance of CSF p-tau235 was comparable to that of other CSF p-tau measurements, indicating its suitability to support a biomarker-based AD diagnosis in clinical settings. Alzheimer’s disease CSF Biomarkers p-tau235 p-tau181 p-tau217 Neurosciences. Biological psychiatry. Neuropsychiatry Neurology. Diseases of the nervous system Agathe Vrillon verfasserin aut Aida Fernández-Lebrero verfasserin aut Paula Ortiz-Romero verfasserin aut Anniina Snellman verfasserin aut Laia Montoliu-Gaya verfasserin aut Wagner S. Brum verfasserin aut Emmanuel Cognat verfasserin aut Julien Dumurgier verfasserin aut Albert Puig-Pijoan verfasserin aut Irene Navalpotro-Gómez verfasserin aut Greta García-Escobar verfasserin aut Thomas K. Karikari verfasserin aut Eugeen Vanmechelen verfasserin aut Nicholas J. Ashton verfasserin aut Henrik Zetterberg verfasserin aut Marc Suárez-Calvet verfasserin aut Claire Paquet verfasserin aut Kaj Blennow verfasserin aut In Alzheimer’s Research & Therapy BMC, 2015 15(2023), 1, Seite 15 (DE-627)605683557 (DE-600)2506521-X 17589193 nnns volume:15 year:2023 number:1 pages:15 https://doi.org/10.1186/s13195-023-01201-0 kostenfrei https://doaj.org/article/77904aa0f595409998732159a64f7f99 kostenfrei https://doi.org/10.1186/s13195-023-01201-0 kostenfrei https://doaj.org/toc/1758-9193 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2023 1 15
spelling	10.1186/s13195-023-01201-0 doi (DE-627)DOAJ087766833 (DE-599)DOAJ77904aa0f595409998732159a64f7f99 DE-627 ger DE-627 rakwb eng RC321-571 RC346-429 Juan Lantero-Rodriguez verfasserin aut Clinical performance and head-to-head comparison of CSF p-tau235 with p-tau181, p-tau217 and p-tau231 in two memory clinic cohorts 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Cerebrospinal fluid (CSF) p-tau235 is a novel biomarker highly specific of Alzheimer’s disease (AD). However, CSF p-tau235 has only been studied in well-characterized research cohorts, which do not fully reflect the patient landscape found in clinical settings. Therefore, in this multicentre study, we investigated the performance of CSF p-tau235 to detect symptomatic AD in clinical settings and compared it with CSF p-tau181, p-tau217 and p-tau231. Methods CSF p-tau235 was measured using an in-house single molecule array (Simoa) assay in two independent memory clinic cohorts: Paris cohort (Lariboisière Fernand-Widal University Hospital Paris, France; n=212) and BIODEGMAR cohort (Hospital del Mar, Barcelona, Spain; n=175). Patients were classified by the syndromic diagnosis (cognitively unimpaired [CU], mild cognitive impairment [MCI] or dementia) and their biological diagnosis (amyloid-beta [Aβ]+ or Aβ $$-$$ - ). Both cohorts included detailed cognitive assessments and CSF biomarker measurements (clinically validated core AD biomarkers [Lumipulse CSF Aβ1–42/40 ratio, p-tau181 and t-tau] and in-house developed Simoa CSF p-tau181, p-tau217 and p-tau231). Results High CSF p-tau235 levels were strongly associated with CSF amyloidosis regardless of the clinical diagnosis, being significantly increased in MCI Aβ+ and dementia Aβ+ when compared with all other Aβ− groups (Paris cohort: P ˂0.0001 for all; BIODEGMAR cohort: P ˂0.05 for all). CSF p-tau235 was pronouncedly increased in the A+T+ profile group compared with A−T− and A+T− groups (P ˂0.0001 for all). Moreover, CSF p-tau235 demonstrated high diagnostic accuracies identifying CSF amyloidosis in symptomatic cases (AUCs=0.86 to 0.96) and discriminating AT groups (AUCs=0.79 to 0.98). Overall, CSF p-tau235 showed similar performances to CSF p-tau181 and CSF p-tau231 when discriminating CSF amyloidosis in various scenarios, but lower than CSF p-tau217. Finally, CSF p-tau235 associated with global cognition and memory domain in both cohorts. Conclusions CSF p-tau235 was increased with the presence of CSF amyloidosis in two independent memory clinic cohorts. CSF p-tau235 accurately identified AD in both MCI and dementia patients. Overall, the diagnostic performance of CSF p-tau235 was comparable to that of other CSF p-tau measurements, indicating its suitability to support a biomarker-based AD diagnosis in clinical settings. Alzheimer’s disease CSF Biomarkers p-tau235 p-tau181 p-tau217 Neurosciences. Biological psychiatry. Neuropsychiatry Neurology. Diseases of the nervous system Agathe Vrillon verfasserin aut Aida Fernández-Lebrero verfasserin aut Paula Ortiz-Romero verfasserin aut Anniina Snellman verfasserin aut Laia Montoliu-Gaya verfasserin aut Wagner S. Brum verfasserin aut Emmanuel Cognat verfasserin aut Julien Dumurgier verfasserin aut Albert Puig-Pijoan verfasserin aut Irene Navalpotro-Gómez verfasserin aut Greta García-Escobar verfasserin aut Thomas K. Karikari verfasserin aut Eugeen Vanmechelen verfasserin aut Nicholas J. Ashton verfasserin aut Henrik Zetterberg verfasserin aut Marc Suárez-Calvet verfasserin aut Claire Paquet verfasserin aut Kaj Blennow verfasserin aut In Alzheimer’s Research & Therapy BMC, 2015 15(2023), 1, Seite 15 (DE-627)605683557 (DE-600)2506521-X 17589193 nnns volume:15 year:2023 number:1 pages:15 https://doi.org/10.1186/s13195-023-01201-0 kostenfrei https://doaj.org/article/77904aa0f595409998732159a64f7f99 kostenfrei https://doi.org/10.1186/s13195-023-01201-0 kostenfrei https://doaj.org/toc/1758-9193 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2023 1 15
allfields_unstemmed	10.1186/s13195-023-01201-0 doi (DE-627)DOAJ087766833 (DE-599)DOAJ77904aa0f595409998732159a64f7f99 DE-627 ger DE-627 rakwb eng RC321-571 RC346-429 Juan Lantero-Rodriguez verfasserin aut Clinical performance and head-to-head comparison of CSF p-tau235 with p-tau181, p-tau217 and p-tau231 in two memory clinic cohorts 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Cerebrospinal fluid (CSF) p-tau235 is a novel biomarker highly specific of Alzheimer’s disease (AD). However, CSF p-tau235 has only been studied in well-characterized research cohorts, which do not fully reflect the patient landscape found in clinical settings. Therefore, in this multicentre study, we investigated the performance of CSF p-tau235 to detect symptomatic AD in clinical settings and compared it with CSF p-tau181, p-tau217 and p-tau231. Methods CSF p-tau235 was measured using an in-house single molecule array (Simoa) assay in two independent memory clinic cohorts: Paris cohort (Lariboisière Fernand-Widal University Hospital Paris, France; n=212) and BIODEGMAR cohort (Hospital del Mar, Barcelona, Spain; n=175). Patients were classified by the syndromic diagnosis (cognitively unimpaired [CU], mild cognitive impairment [MCI] or dementia) and their biological diagnosis (amyloid-beta [Aβ]+ or Aβ $$-$$ - ). Both cohorts included detailed cognitive assessments and CSF biomarker measurements (clinically validated core AD biomarkers [Lumipulse CSF Aβ1–42/40 ratio, p-tau181 and t-tau] and in-house developed Simoa CSF p-tau181, p-tau217 and p-tau231). Results High CSF p-tau235 levels were strongly associated with CSF amyloidosis regardless of the clinical diagnosis, being significantly increased in MCI Aβ+ and dementia Aβ+ when compared with all other Aβ− groups (Paris cohort: P ˂0.0001 for all; BIODEGMAR cohort: P ˂0.05 for all). CSF p-tau235 was pronouncedly increased in the A+T+ profile group compared with A−T− and A+T− groups (P ˂0.0001 for all). Moreover, CSF p-tau235 demonstrated high diagnostic accuracies identifying CSF amyloidosis in symptomatic cases (AUCs=0.86 to 0.96) and discriminating AT groups (AUCs=0.79 to 0.98). Overall, CSF p-tau235 showed similar performances to CSF p-tau181 and CSF p-tau231 when discriminating CSF amyloidosis in various scenarios, but lower than CSF p-tau217. Finally, CSF p-tau235 associated with global cognition and memory domain in both cohorts. Conclusions CSF p-tau235 was increased with the presence of CSF amyloidosis in two independent memory clinic cohorts. CSF p-tau235 accurately identified AD in both MCI and dementia patients. Overall, the diagnostic performance of CSF p-tau235 was comparable to that of other CSF p-tau measurements, indicating its suitability to support a biomarker-based AD diagnosis in clinical settings. Alzheimer’s disease CSF Biomarkers p-tau235 p-tau181 p-tau217 Neurosciences. Biological psychiatry. Neuropsychiatry Neurology. Diseases of the nervous system Agathe Vrillon verfasserin aut Aida Fernández-Lebrero verfasserin aut Paula Ortiz-Romero verfasserin aut Anniina Snellman verfasserin aut Laia Montoliu-Gaya verfasserin aut Wagner S. Brum verfasserin aut Emmanuel Cognat verfasserin aut Julien Dumurgier verfasserin aut Albert Puig-Pijoan verfasserin aut Irene Navalpotro-Gómez verfasserin aut Greta García-Escobar verfasserin aut Thomas K. Karikari verfasserin aut Eugeen Vanmechelen verfasserin aut Nicholas J. Ashton verfasserin aut Henrik Zetterberg verfasserin aut Marc Suárez-Calvet verfasserin aut Claire Paquet verfasserin aut Kaj Blennow verfasserin aut In Alzheimer’s Research & Therapy BMC, 2015 15(2023), 1, Seite 15 (DE-627)605683557 (DE-600)2506521-X 17589193 nnns volume:15 year:2023 number:1 pages:15 https://doi.org/10.1186/s13195-023-01201-0 kostenfrei https://doaj.org/article/77904aa0f595409998732159a64f7f99 kostenfrei https://doi.org/10.1186/s13195-023-01201-0 kostenfrei https://doaj.org/toc/1758-9193 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2023 1 15
allfieldsGer	10.1186/s13195-023-01201-0 doi (DE-627)DOAJ087766833 (DE-599)DOAJ77904aa0f595409998732159a64f7f99 DE-627 ger DE-627 rakwb eng RC321-571 RC346-429 Juan Lantero-Rodriguez verfasserin aut Clinical performance and head-to-head comparison of CSF p-tau235 with p-tau181, p-tau217 and p-tau231 in two memory clinic cohorts 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Cerebrospinal fluid (CSF) p-tau235 is a novel biomarker highly specific of Alzheimer’s disease (AD). However, CSF p-tau235 has only been studied in well-characterized research cohorts, which do not fully reflect the patient landscape found in clinical settings. Therefore, in this multicentre study, we investigated the performance of CSF p-tau235 to detect symptomatic AD in clinical settings and compared it with CSF p-tau181, p-tau217 and p-tau231. Methods CSF p-tau235 was measured using an in-house single molecule array (Simoa) assay in two independent memory clinic cohorts: Paris cohort (Lariboisière Fernand-Widal University Hospital Paris, France; n=212) and BIODEGMAR cohort (Hospital del Mar, Barcelona, Spain; n=175). Patients were classified by the syndromic diagnosis (cognitively unimpaired [CU], mild cognitive impairment [MCI] or dementia) and their biological diagnosis (amyloid-beta [Aβ]+ or Aβ $$-$$ - ). Both cohorts included detailed cognitive assessments and CSF biomarker measurements (clinically validated core AD biomarkers [Lumipulse CSF Aβ1–42/40 ratio, p-tau181 and t-tau] and in-house developed Simoa CSF p-tau181, p-tau217 and p-tau231). Results High CSF p-tau235 levels were strongly associated with CSF amyloidosis regardless of the clinical diagnosis, being significantly increased in MCI Aβ+ and dementia Aβ+ when compared with all other Aβ− groups (Paris cohort: P ˂0.0001 for all; BIODEGMAR cohort: P ˂0.05 for all). CSF p-tau235 was pronouncedly increased in the A+T+ profile group compared with A−T− and A+T− groups (P ˂0.0001 for all). Moreover, CSF p-tau235 demonstrated high diagnostic accuracies identifying CSF amyloidosis in symptomatic cases (AUCs=0.86 to 0.96) and discriminating AT groups (AUCs=0.79 to 0.98). Overall, CSF p-tau235 showed similar performances to CSF p-tau181 and CSF p-tau231 when discriminating CSF amyloidosis in various scenarios, but lower than CSF p-tau217. Finally, CSF p-tau235 associated with global cognition and memory domain in both cohorts. Conclusions CSF p-tau235 was increased with the presence of CSF amyloidosis in two independent memory clinic cohorts. CSF p-tau235 accurately identified AD in both MCI and dementia patients. Overall, the diagnostic performance of CSF p-tau235 was comparable to that of other CSF p-tau measurements, indicating its suitability to support a biomarker-based AD diagnosis in clinical settings. Alzheimer’s disease CSF Biomarkers p-tau235 p-tau181 p-tau217 Neurosciences. Biological psychiatry. Neuropsychiatry Neurology. Diseases of the nervous system Agathe Vrillon verfasserin aut Aida Fernández-Lebrero verfasserin aut Paula Ortiz-Romero verfasserin aut Anniina Snellman verfasserin aut Laia Montoliu-Gaya verfasserin aut Wagner S. Brum verfasserin aut Emmanuel Cognat verfasserin aut Julien Dumurgier verfasserin aut Albert Puig-Pijoan verfasserin aut Irene Navalpotro-Gómez verfasserin aut Greta García-Escobar verfasserin aut Thomas K. Karikari verfasserin aut Eugeen Vanmechelen verfasserin aut Nicholas J. Ashton verfasserin aut Henrik Zetterberg verfasserin aut Marc Suárez-Calvet verfasserin aut Claire Paquet verfasserin aut Kaj Blennow verfasserin aut In Alzheimer’s Research & Therapy BMC, 2015 15(2023), 1, Seite 15 (DE-627)605683557 (DE-600)2506521-X 17589193 nnns volume:15 year:2023 number:1 pages:15 https://doi.org/10.1186/s13195-023-01201-0 kostenfrei https://doaj.org/article/77904aa0f595409998732159a64f7f99 kostenfrei https://doi.org/10.1186/s13195-023-01201-0 kostenfrei https://doaj.org/toc/1758-9193 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2023 1 15
allfieldsSound	10.1186/s13195-023-01201-0 doi (DE-627)DOAJ087766833 (DE-599)DOAJ77904aa0f595409998732159a64f7f99 DE-627 ger DE-627 rakwb eng RC321-571 RC346-429 Juan Lantero-Rodriguez verfasserin aut Clinical performance and head-to-head comparison of CSF p-tau235 with p-tau181, p-tau217 and p-tau231 in two memory clinic cohorts 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Cerebrospinal fluid (CSF) p-tau235 is a novel biomarker highly specific of Alzheimer’s disease (AD). However, CSF p-tau235 has only been studied in well-characterized research cohorts, which do not fully reflect the patient landscape found in clinical settings. Therefore, in this multicentre study, we investigated the performance of CSF p-tau235 to detect symptomatic AD in clinical settings and compared it with CSF p-tau181, p-tau217 and p-tau231. Methods CSF p-tau235 was measured using an in-house single molecule array (Simoa) assay in two independent memory clinic cohorts: Paris cohort (Lariboisière Fernand-Widal University Hospital Paris, France; n=212) and BIODEGMAR cohort (Hospital del Mar, Barcelona, Spain; n=175). Patients were classified by the syndromic diagnosis (cognitively unimpaired [CU], mild cognitive impairment [MCI] or dementia) and their biological diagnosis (amyloid-beta [Aβ]+ or Aβ $$-$$ - ). Both cohorts included detailed cognitive assessments and CSF biomarker measurements (clinically validated core AD biomarkers [Lumipulse CSF Aβ1–42/40 ratio, p-tau181 and t-tau] and in-house developed Simoa CSF p-tau181, p-tau217 and p-tau231). Results High CSF p-tau235 levels were strongly associated with CSF amyloidosis regardless of the clinical diagnosis, being significantly increased in MCI Aβ+ and dementia Aβ+ when compared with all other Aβ− groups (Paris cohort: P ˂0.0001 for all; BIODEGMAR cohort: P ˂0.05 for all). CSF p-tau235 was pronouncedly increased in the A+T+ profile group compared with A−T− and A+T− groups (P ˂0.0001 for all). Moreover, CSF p-tau235 demonstrated high diagnostic accuracies identifying CSF amyloidosis in symptomatic cases (AUCs=0.86 to 0.96) and discriminating AT groups (AUCs=0.79 to 0.98). Overall, CSF p-tau235 showed similar performances to CSF p-tau181 and CSF p-tau231 when discriminating CSF amyloidosis in various scenarios, but lower than CSF p-tau217. Finally, CSF p-tau235 associated with global cognition and memory domain in both cohorts. Conclusions CSF p-tau235 was increased with the presence of CSF amyloidosis in two independent memory clinic cohorts. CSF p-tau235 accurately identified AD in both MCI and dementia patients. Overall, the diagnostic performance of CSF p-tau235 was comparable to that of other CSF p-tau measurements, indicating its suitability to support a biomarker-based AD diagnosis in clinical settings. Alzheimer’s disease CSF Biomarkers p-tau235 p-tau181 p-tau217 Neurosciences. Biological psychiatry. Neuropsychiatry Neurology. Diseases of the nervous system Agathe Vrillon verfasserin aut Aida Fernández-Lebrero verfasserin aut Paula Ortiz-Romero verfasserin aut Anniina Snellman verfasserin aut Laia Montoliu-Gaya verfasserin aut Wagner S. Brum verfasserin aut Emmanuel Cognat verfasserin aut Julien Dumurgier verfasserin aut Albert Puig-Pijoan verfasserin aut Irene Navalpotro-Gómez verfasserin aut Greta García-Escobar verfasserin aut Thomas K. Karikari verfasserin aut Eugeen Vanmechelen verfasserin aut Nicholas J. Ashton verfasserin aut Henrik Zetterberg verfasserin aut Marc Suárez-Calvet verfasserin aut Claire Paquet verfasserin aut Kaj Blennow verfasserin aut In Alzheimer’s Research & Therapy BMC, 2015 15(2023), 1, Seite 15 (DE-627)605683557 (DE-600)2506521-X 17589193 nnns volume:15 year:2023 number:1 pages:15 https://doi.org/10.1186/s13195-023-01201-0 kostenfrei https://doaj.org/article/77904aa0f595409998732159a64f7f99 kostenfrei https://doi.org/10.1186/s13195-023-01201-0 kostenfrei https://doaj.org/toc/1758-9193 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2023 1 15
language	English
source	In Alzheimer’s Research & Therapy 15(2023), 1, Seite 15 volume:15 year:2023 number:1 pages:15
sourceStr	In Alzheimer’s Research & Therapy 15(2023), 1, Seite 15 volume:15 year:2023 number:1 pages:15
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topic_facet	Alzheimer’s disease CSF Biomarkers p-tau235 p-tau181 p-tau217 Neurosciences. Biological psychiatry. Neuropsychiatry Neurology. Diseases of the nervous system
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container_title	Alzheimer’s Research & Therapy
authorswithroles_txt_mv	Juan Lantero-Rodriguez @@aut@@ Agathe Vrillon @@aut@@ Aida Fernández-Lebrero @@aut@@ Paula Ortiz-Romero @@aut@@ Anniina Snellman @@aut@@ Laia Montoliu-Gaya @@aut@@ Wagner S. Brum @@aut@@ Emmanuel Cognat @@aut@@ Julien Dumurgier @@aut@@ Albert Puig-Pijoan @@aut@@ Irene Navalpotro-Gómez @@aut@@ Greta García-Escobar @@aut@@ Thomas K. Karikari @@aut@@ Eugeen Vanmechelen @@aut@@ Nicholas J. Ashton @@aut@@ Henrik Zetterberg @@aut@@ Marc Suárez-Calvet @@aut@@ Claire Paquet @@aut@@ Kaj Blennow @@aut@@
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However, CSF p-tau235 has only been studied in well-characterized research cohorts, which do not fully reflect the patient landscape found in clinical settings. Therefore, in this multicentre study, we investigated the performance of CSF p-tau235 to detect symptomatic AD in clinical settings and compared it with CSF p-tau181, p-tau217 and p-tau231. Methods CSF p-tau235 was measured using an in-house single molecule array (Simoa) assay in two independent memory clinic cohorts: Paris cohort (Lariboisière Fernand-Widal University Hospital Paris, France; n=212) and BIODEGMAR cohort (Hospital del Mar, Barcelona, Spain; n=175). Patients were classified by the syndromic diagnosis (cognitively unimpaired [CU], mild cognitive impairment [MCI] or dementia) and their biological diagnosis (amyloid-beta [Aβ]+ or Aβ $$-$$ - ). Both cohorts included detailed cognitive assessments and CSF biomarker measurements (clinically validated core AD biomarkers [Lumipulse CSF Aβ1–42/40 ratio, p-tau181 and t-tau] and in-house developed Simoa CSF p-tau181, p-tau217 and p-tau231). Results High CSF p-tau235 levels were strongly associated with CSF amyloidosis regardless of the clinical diagnosis, being significantly increased in MCI Aβ+ and dementia Aβ+ when compared with all other Aβ− groups (Paris cohort: P ˂0.0001 for all; BIODEGMAR cohort: P ˂0.05 for all). CSF p-tau235 was pronouncedly increased in the A+T+ profile group compared with A−T− and A+T− groups (P ˂0.0001 for all). Moreover, CSF p-tau235 demonstrated high diagnostic accuracies identifying CSF amyloidosis in symptomatic cases (AUCs=0.86 to 0.96) and discriminating AT groups (AUCs=0.79 to 0.98). Overall, CSF p-tau235 showed similar performances to CSF p-tau181 and CSF p-tau231 when discriminating CSF amyloidosis in various scenarios, but lower than CSF p-tau217. Finally, CSF p-tau235 associated with global cognition and memory domain in both cohorts. Conclusions CSF p-tau235 was increased with the presence of CSF amyloidosis in two independent memory clinic cohorts. CSF p-tau235 accurately identified AD in both MCI and dementia patients. Overall, the diagnostic performance of CSF p-tau235 was comparable to that of other CSF p-tau measurements, indicating its suitability to support a biomarker-based AD diagnosis in clinical settings.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Alzheimer’s disease</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">CSF</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Biomarkers</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">p-tau235</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">p-tau181</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">p-tau217</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Neurosciences. Biological psychiatry. Neuropsychiatry</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Neurology. 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callnumber-first	R - Medicine
author	Juan Lantero-Rodriguez
spellingShingle	Juan Lantero-Rodriguez misc RC321-571 misc RC346-429 misc Alzheimer’s disease misc CSF misc Biomarkers misc p-tau235 misc p-tau181 misc p-tau217 misc Neurosciences. Biological psychiatry. Neuropsychiatry misc Neurology. Diseases of the nervous system Clinical performance and head-to-head comparison of CSF p-tau235 with p-tau181, p-tau217 and p-tau231 in two memory clinic cohorts
authorStr	Juan Lantero-Rodriguez
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topic_title	RC321-571 RC346-429 Clinical performance and head-to-head comparison of CSF p-tau235 with p-tau181, p-tau217 and p-tau231 in two memory clinic cohorts Alzheimer’s disease CSF Biomarkers p-tau235 p-tau181 p-tau217
topic	misc RC321-571 misc RC346-429 misc Alzheimer’s disease misc CSF misc Biomarkers misc p-tau235 misc p-tau181 misc p-tau217 misc Neurosciences. Biological psychiatry. Neuropsychiatry misc Neurology. Diseases of the nervous system
topic_unstemmed	misc RC321-571 misc RC346-429 misc Alzheimer’s disease misc CSF misc Biomarkers misc p-tau235 misc p-tau181 misc p-tau217 misc Neurosciences. Biological psychiatry. Neuropsychiatry misc Neurology. Diseases of the nervous system
topic_browse	misc RC321-571 misc RC346-429 misc Alzheimer’s disease misc CSF misc Biomarkers misc p-tau235 misc p-tau181 misc p-tau217 misc Neurosciences. Biological psychiatry. Neuropsychiatry misc Neurology. Diseases of the nervous system
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title	Clinical performance and head-to-head comparison of CSF p-tau235 with p-tau181, p-tau217 and p-tau231 in two memory clinic cohorts
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title_full	Clinical performance and head-to-head comparison of CSF p-tau235 with p-tau181, p-tau217 and p-tau231 in two memory clinic cohorts
author_sort	Juan Lantero-Rodriguez
journal	Alzheimer’s Research & Therapy
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author_browse	Juan Lantero-Rodriguez Agathe Vrillon Aida Fernández-Lebrero Paula Ortiz-Romero Anniina Snellman Laia Montoliu-Gaya Wagner S. Brum Emmanuel Cognat Julien Dumurgier Albert Puig-Pijoan Irene Navalpotro-Gómez Greta García-Escobar Thomas K. Karikari Eugeen Vanmechelen Nicholas J. Ashton Henrik Zetterberg Marc Suárez-Calvet Claire Paquet Kaj Blennow
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title_sort	clinical performance and head-to-head comparison of csf p-tau235 with p-tau181, p-tau217 and p-tau231 in two memory clinic cohorts
callnumber	RC321-571
title_auth	Clinical performance and head-to-head comparison of CSF p-tau235 with p-tau181, p-tau217 and p-tau231 in two memory clinic cohorts
abstract	Abstract Background Cerebrospinal fluid (CSF) p-tau235 is a novel biomarker highly specific of Alzheimer’s disease (AD). However, CSF p-tau235 has only been studied in well-characterized research cohorts, which do not fully reflect the patient landscape found in clinical settings. Therefore, in this multicentre study, we investigated the performance of CSF p-tau235 to detect symptomatic AD in clinical settings and compared it with CSF p-tau181, p-tau217 and p-tau231. Methods CSF p-tau235 was measured using an in-house single molecule array (Simoa) assay in two independent memory clinic cohorts: Paris cohort (Lariboisière Fernand-Widal University Hospital Paris, France; n=212) and BIODEGMAR cohort (Hospital del Mar, Barcelona, Spain; n=175). Patients were classified by the syndromic diagnosis (cognitively unimpaired [CU], mild cognitive impairment [MCI] or dementia) and their biological diagnosis (amyloid-beta [Aβ]+ or Aβ $$-$$ - ). Both cohorts included detailed cognitive assessments and CSF biomarker measurements (clinically validated core AD biomarkers [Lumipulse CSF Aβ1–42/40 ratio, p-tau181 and t-tau] and in-house developed Simoa CSF p-tau181, p-tau217 and p-tau231). Results High CSF p-tau235 levels were strongly associated with CSF amyloidosis regardless of the clinical diagnosis, being significantly increased in MCI Aβ+ and dementia Aβ+ when compared with all other Aβ− groups (Paris cohort: P ˂0.0001 for all; BIODEGMAR cohort: P ˂0.05 for all). CSF p-tau235 was pronouncedly increased in the A+T+ profile group compared with A−T− and A+T− groups (P ˂0.0001 for all). Moreover, CSF p-tau235 demonstrated high diagnostic accuracies identifying CSF amyloidosis in symptomatic cases (AUCs=0.86 to 0.96) and discriminating AT groups (AUCs=0.79 to 0.98). Overall, CSF p-tau235 showed similar performances to CSF p-tau181 and CSF p-tau231 when discriminating CSF amyloidosis in various scenarios, but lower than CSF p-tau217. Finally, CSF p-tau235 associated with global cognition and memory domain in both cohorts. Conclusions CSF p-tau235 was increased with the presence of CSF amyloidosis in two independent memory clinic cohorts. CSF p-tau235 accurately identified AD in both MCI and dementia patients. Overall, the diagnostic performance of CSF p-tau235 was comparable to that of other CSF p-tau measurements, indicating its suitability to support a biomarker-based AD diagnosis in clinical settings.
abstractGer	Abstract Background Cerebrospinal fluid (CSF) p-tau235 is a novel biomarker highly specific of Alzheimer’s disease (AD). However, CSF p-tau235 has only been studied in well-characterized research cohorts, which do not fully reflect the patient landscape found in clinical settings. Therefore, in this multicentre study, we investigated the performance of CSF p-tau235 to detect symptomatic AD in clinical settings and compared it with CSF p-tau181, p-tau217 and p-tau231. Methods CSF p-tau235 was measured using an in-house single molecule array (Simoa) assay in two independent memory clinic cohorts: Paris cohort (Lariboisière Fernand-Widal University Hospital Paris, France; n=212) and BIODEGMAR cohort (Hospital del Mar, Barcelona, Spain; n=175). Patients were classified by the syndromic diagnosis (cognitively unimpaired [CU], mild cognitive impairment [MCI] or dementia) and their biological diagnosis (amyloid-beta [Aβ]+ or Aβ $$-$$ - ). Both cohorts included detailed cognitive assessments and CSF biomarker measurements (clinically validated core AD biomarkers [Lumipulse CSF Aβ1–42/40 ratio, p-tau181 and t-tau] and in-house developed Simoa CSF p-tau181, p-tau217 and p-tau231). Results High CSF p-tau235 levels were strongly associated with CSF amyloidosis regardless of the clinical diagnosis, being significantly increased in MCI Aβ+ and dementia Aβ+ when compared with all other Aβ− groups (Paris cohort: P ˂0.0001 for all; BIODEGMAR cohort: P ˂0.05 for all). CSF p-tau235 was pronouncedly increased in the A+T+ profile group compared with A−T− and A+T− groups (P ˂0.0001 for all). Moreover, CSF p-tau235 demonstrated high diagnostic accuracies identifying CSF amyloidosis in symptomatic cases (AUCs=0.86 to 0.96) and discriminating AT groups (AUCs=0.79 to 0.98). Overall, CSF p-tau235 showed similar performances to CSF p-tau181 and CSF p-tau231 when discriminating CSF amyloidosis in various scenarios, but lower than CSF p-tau217. Finally, CSF p-tau235 associated with global cognition and memory domain in both cohorts. Conclusions CSF p-tau235 was increased with the presence of CSF amyloidosis in two independent memory clinic cohorts. CSF p-tau235 accurately identified AD in both MCI and dementia patients. Overall, the diagnostic performance of CSF p-tau235 was comparable to that of other CSF p-tau measurements, indicating its suitability to support a biomarker-based AD diagnosis in clinical settings.
abstract_unstemmed	Abstract Background Cerebrospinal fluid (CSF) p-tau235 is a novel biomarker highly specific of Alzheimer’s disease (AD). However, CSF p-tau235 has only been studied in well-characterized research cohorts, which do not fully reflect the patient landscape found in clinical settings. Therefore, in this multicentre study, we investigated the performance of CSF p-tau235 to detect symptomatic AD in clinical settings and compared it with CSF p-tau181, p-tau217 and p-tau231. Methods CSF p-tau235 was measured using an in-house single molecule array (Simoa) assay in two independent memory clinic cohorts: Paris cohort (Lariboisière Fernand-Widal University Hospital Paris, France; n=212) and BIODEGMAR cohort (Hospital del Mar, Barcelona, Spain; n=175). Patients were classified by the syndromic diagnosis (cognitively unimpaired [CU], mild cognitive impairment [MCI] or dementia) and their biological diagnosis (amyloid-beta [Aβ]+ or Aβ $$-$$ - ). Both cohorts included detailed cognitive assessments and CSF biomarker measurements (clinically validated core AD biomarkers [Lumipulse CSF Aβ1–42/40 ratio, p-tau181 and t-tau] and in-house developed Simoa CSF p-tau181, p-tau217 and p-tau231). Results High CSF p-tau235 levels were strongly associated with CSF amyloidosis regardless of the clinical diagnosis, being significantly increased in MCI Aβ+ and dementia Aβ+ when compared with all other Aβ− groups (Paris cohort: P ˂0.0001 for all; BIODEGMAR cohort: P ˂0.05 for all). CSF p-tau235 was pronouncedly increased in the A+T+ profile group compared with A−T− and A+T− groups (P ˂0.0001 for all). Moreover, CSF p-tau235 demonstrated high diagnostic accuracies identifying CSF amyloidosis in symptomatic cases (AUCs=0.86 to 0.96) and discriminating AT groups (AUCs=0.79 to 0.98). Overall, CSF p-tau235 showed similar performances to CSF p-tau181 and CSF p-tau231 when discriminating CSF amyloidosis in various scenarios, but lower than CSF p-tau217. Finally, CSF p-tau235 associated with global cognition and memory domain in both cohorts. Conclusions CSF p-tau235 was increased with the presence of CSF amyloidosis in two independent memory clinic cohorts. CSF p-tau235 accurately identified AD in both MCI and dementia patients. Overall, the diagnostic performance of CSF p-tau235 was comparable to that of other CSF p-tau measurements, indicating its suitability to support a biomarker-based AD diagnosis in clinical settings.
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title_short	Clinical performance and head-to-head comparison of CSF p-tau235 with p-tau181, p-tau217 and p-tau231 in two memory clinic cohorts
url	https://doi.org/10.1186/s13195-023-01201-0 https://doaj.org/article/77904aa0f595409998732159a64f7f99 https://doaj.org/toc/1758-9193
remote_bool	true
author2	Agathe Vrillon Aida Fernández-Lebrero Paula Ortiz-Romero Anniina Snellman Laia Montoliu-Gaya Wagner S. Brum Emmanuel Cognat Julien Dumurgier Albert Puig-Pijoan Irene Navalpotro-Gómez Greta García-Escobar Thomas K. Karikari Eugeen Vanmechelen Nicholas J. Ashton Henrik Zetterberg Marc Suárez-Calvet Claire Paquet Kaj Blennow
author2Str	Agathe Vrillon Aida Fernández-Lebrero Paula Ortiz-Romero Anniina Snellman Laia Montoliu-Gaya Wagner S. Brum Emmanuel Cognat Julien Dumurgier Albert Puig-Pijoan Irene Navalpotro-Gómez Greta García-Escobar Thomas K. Karikari Eugeen Vanmechelen Nicholas J. Ashton Henrik Zetterberg Marc Suárez-Calvet Claire Paquet Kaj Blennow
ppnlink	605683557
callnumber-subject	RC - Internal Medicine
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isOA_txt	true
hochschulschrift_bool	false
doi_str	10.1186/s13195-023-01201-0
callnumber-a	RC321-571
up_date	2024-07-03T13:50:12.556Z
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Clinical performance and head-to-head comparison of CSF p-tau235 with p-tau181, p-tau217 and p-tau231 in two memory clinic cohorts

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