Serum neurofilament light chain levels reflect cortical neurodegeneration in de novo Parkinson's disease

Introduction: Cognitive impairment and dementia are highly prevalent non-motor complications in Parkinson's disease (PD) with deleterious consequences for patients and caregivers. With no treatment currently available, finding and validating minimally-invasive biomarkers of neurodegeneration in...
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Autor*in:	Sampedro, Frederic [verfasserIn] Pérez-González, Rocío [verfasserIn] Martínez-Horta, Saul [verfasserIn] Marín-Lahoz, Juan [verfasserIn] Pagonabarraga, Javier [verfasserIn] Kulisevsky, Jaime [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	Parkinson's disease Biomarkers Cognitive decline NfL Cortical thinning

Übergeordnetes Werk:	Enthalten in: Parkinsonism & related disorders - Amsterdam [u.a.] : Elsevier Science, 1995, 74, Seite 43-49
Übergeordnetes Werk:	volume:74 ; pages:43-49

DOI / URN:	10.1016/j.parkreldis.2020.04.009

Katalog-ID:	ELV004288823

Internformat


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100	1		\|a Sampedro, Frederic \|e verfasserin \|4 aut
245	1	0	\|a Serum neurofilament light chain levels reflect cortical neurodegeneration in de novo Parkinson's disease
264		1	\|c 2020
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520			\|a Introduction: Cognitive impairment and dementia are highly prevalent non-motor complications in Parkinson's disease (PD) with deleterious consequences for patients and caregivers. With no treatment currently available, finding and validating minimally-invasive biomarkers of neurodegeneration in this population represents an urgent need for clinical trials targeting its prevention or delay. Recently, serum neurofilament light chain (NfL) levels have been identified as a promising biomarker of neural loss, but whether they reflect cortical neurodegeneration in early PD stages has not been addressed.Methods: From the Parkinson's Progression Markers Initiative (PPMI), we selected 133 de novo PD patients and 56 healthy controls (HC) with available structural neuroimaging and serum NfL data. We then studied whether NfL levels were abnormal in the PD group with respect to HC, and whether they correlated with cognitive indicators and cortical macro (cortical thinning) and microstructural (increased intracortical mean diffusivity) degeneration.Results: Serum NfL levels were significantly increased in the PD group (p = 0.010), and were also related to worse cognitive performance and a cortical macro and microstructural compromise (p < 0.05 corrected). These associations were observed both cross-sectionally and longitudinally within a one-year follow-up period. Topographically, NfL levels reflected posterior-cortical deterioration rather than frontal damage. Importantly, NfL levels were not associated with striatal SPECT-DAT uptake or β-amyloid burden.Discussion: Our results show that serum NfL levels reflect cortical neurodegeneration from the very early stages of PD. Moreover, its brain structural correlates and its lack of relationship with dopaminergic depletion or amyloidosis suggests that NfL could track the underlying pathological process leading to PD dementia.
650		4	\|a Parkinson's disease
650		4	\|a Biomarkers
650		4	\|a Cognitive decline
650		4	\|a NfL
650		4	\|a Cortical thinning
700	1		\|a Pérez-González, Rocío \|e verfasserin \|4 aut
700	1		\|a Martínez-Horta, Saul \|e verfasserin \|4 aut
700	1		\|a Marín-Lahoz, Juan \|e verfasserin \|4 aut
700	1		\|a Pagonabarraga, Javier \|e verfasserin \|4 aut
700	1		\|a Kulisevsky, Jaime \|e verfasserin \|4 aut
773	0	8	\|i Enthalten in \|t Parkinsonism & related disorders \|d Amsterdam [u.a.] : Elsevier Science, 1995 \|g 74, Seite 43-49 \|h Online-Ressource \|w (DE-627)32448898X \|w (DE-600)2027635-7 \|w (DE-576)272349704 \|x 1873-5126 \|7 nnns
773	1	8	\|g volume:74 \|g pages:43-49
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912			\|a GBV_ILN_4046
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912			\|a GBV_ILN_4322
912			\|a GBV_ILN_4323
912			\|a GBV_ILN_4324
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912			\|a GBV_ILN_4333
912			\|a GBV_ILN_4334
912			\|a GBV_ILN_4335
912			\|a GBV_ILN_4338
912			\|a GBV_ILN_4393
936	b	k	\|a 44.90 \|j Neurologie
951			\|a AR
952			\|d 74 \|h 43-49

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publishDate	2020
allfields	10.1016/j.parkreldis.2020.04.009 doi (DE-627)ELV004288823 (ELSEVIER)S1353-8020(20)30104-8 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl Sampedro, Frederic verfasserin aut Serum neurofilament light chain levels reflect cortical neurodegeneration in de novo Parkinson's disease 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction: Cognitive impairment and dementia are highly prevalent non-motor complications in Parkinson's disease (PD) with deleterious consequences for patients and caregivers. With no treatment currently available, finding and validating minimally-invasive biomarkers of neurodegeneration in this population represents an urgent need for clinical trials targeting its prevention or delay. Recently, serum neurofilament light chain (NfL) levels have been identified as a promising biomarker of neural loss, but whether they reflect cortical neurodegeneration in early PD stages has not been addressed.Methods: From the Parkinson's Progression Markers Initiative (PPMI), we selected 133 de novo PD patients and 56 healthy controls (HC) with available structural neuroimaging and serum NfL data. We then studied whether NfL levels were abnormal in the PD group with respect to HC, and whether they correlated with cognitive indicators and cortical macro (cortical thinning) and microstructural (increased intracortical mean diffusivity) degeneration.Results: Serum NfL levels were significantly increased in the PD group (p = 0.010), and were also related to worse cognitive performance and a cortical macro and microstructural compromise (p < 0.05 corrected). These associations were observed both cross-sectionally and longitudinally within a one-year follow-up period. Topographically, NfL levels reflected posterior-cortical deterioration rather than frontal damage. Importantly, NfL levels were not associated with striatal SPECT-DAT uptake or β-amyloid burden.Discussion: Our results show that serum NfL levels reflect cortical neurodegeneration from the very early stages of PD. Moreover, its brain structural correlates and its lack of relationship with dopaminergic depletion or amyloidosis suggests that NfL could track the underlying pathological process leading to PD dementia. Parkinson's disease Biomarkers Cognitive decline NfL Cortical thinning Pérez-González, Rocío verfasserin aut Martínez-Horta, Saul verfasserin aut Marín-Lahoz, Juan verfasserin aut Pagonabarraga, Javier verfasserin aut Kulisevsky, Jaime verfasserin aut Enthalten in Parkinsonism & related disorders Amsterdam [u.a.] : Elsevier Science, 1995 74, Seite 43-49 Online-Ressource (DE-627)32448898X (DE-600)2027635-7 (DE-576)272349704 1873-5126 nnns volume:74 pages:43-49 GBV_USEFLAG_U SYSFLAG_U GBV_ELV GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.90 Neurologie AR 74 43-49
spelling	10.1016/j.parkreldis.2020.04.009 doi (DE-627)ELV004288823 (ELSEVIER)S1353-8020(20)30104-8 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl Sampedro, Frederic verfasserin aut Serum neurofilament light chain levels reflect cortical neurodegeneration in de novo Parkinson's disease 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction: Cognitive impairment and dementia are highly prevalent non-motor complications in Parkinson's disease (PD) with deleterious consequences for patients and caregivers. With no treatment currently available, finding and validating minimally-invasive biomarkers of neurodegeneration in this population represents an urgent need for clinical trials targeting its prevention or delay. Recently, serum neurofilament light chain (NfL) levels have been identified as a promising biomarker of neural loss, but whether they reflect cortical neurodegeneration in early PD stages has not been addressed.Methods: From the Parkinson's Progression Markers Initiative (PPMI), we selected 133 de novo PD patients and 56 healthy controls (HC) with available structural neuroimaging and serum NfL data. We then studied whether NfL levels were abnormal in the PD group with respect to HC, and whether they correlated with cognitive indicators and cortical macro (cortical thinning) and microstructural (increased intracortical mean diffusivity) degeneration.Results: Serum NfL levels were significantly increased in the PD group (p = 0.010), and were also related to worse cognitive performance and a cortical macro and microstructural compromise (p < 0.05 corrected). These associations were observed both cross-sectionally and longitudinally within a one-year follow-up period. Topographically, NfL levels reflected posterior-cortical deterioration rather than frontal damage. Importantly, NfL levels were not associated with striatal SPECT-DAT uptake or β-amyloid burden.Discussion: Our results show that serum NfL levels reflect cortical neurodegeneration from the very early stages of PD. Moreover, its brain structural correlates and its lack of relationship with dopaminergic depletion or amyloidosis suggests that NfL could track the underlying pathological process leading to PD dementia. Parkinson's disease Biomarkers Cognitive decline NfL Cortical thinning Pérez-González, Rocío verfasserin aut Martínez-Horta, Saul verfasserin aut Marín-Lahoz, Juan verfasserin aut Pagonabarraga, Javier verfasserin aut Kulisevsky, Jaime verfasserin aut Enthalten in Parkinsonism & related disorders Amsterdam [u.a.] : Elsevier Science, 1995 74, Seite 43-49 Online-Ressource (DE-627)32448898X (DE-600)2027635-7 (DE-576)272349704 1873-5126 nnns volume:74 pages:43-49 GBV_USEFLAG_U SYSFLAG_U GBV_ELV GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.90 Neurologie AR 74 43-49
allfields_unstemmed	10.1016/j.parkreldis.2020.04.009 doi (DE-627)ELV004288823 (ELSEVIER)S1353-8020(20)30104-8 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl Sampedro, Frederic verfasserin aut Serum neurofilament light chain levels reflect cortical neurodegeneration in de novo Parkinson's disease 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction: Cognitive impairment and dementia are highly prevalent non-motor complications in Parkinson's disease (PD) with deleterious consequences for patients and caregivers. With no treatment currently available, finding and validating minimally-invasive biomarkers of neurodegeneration in this population represents an urgent need for clinical trials targeting its prevention or delay. Recently, serum neurofilament light chain (NfL) levels have been identified as a promising biomarker of neural loss, but whether they reflect cortical neurodegeneration in early PD stages has not been addressed.Methods: From the Parkinson's Progression Markers Initiative (PPMI), we selected 133 de novo PD patients and 56 healthy controls (HC) with available structural neuroimaging and serum NfL data. We then studied whether NfL levels were abnormal in the PD group with respect to HC, and whether they correlated with cognitive indicators and cortical macro (cortical thinning) and microstructural (increased intracortical mean diffusivity) degeneration.Results: Serum NfL levels were significantly increased in the PD group (p = 0.010), and were also related to worse cognitive performance and a cortical macro and microstructural compromise (p < 0.05 corrected). These associations were observed both cross-sectionally and longitudinally within a one-year follow-up period. Topographically, NfL levels reflected posterior-cortical deterioration rather than frontal damage. Importantly, NfL levels were not associated with striatal SPECT-DAT uptake or β-amyloid burden.Discussion: Our results show that serum NfL levels reflect cortical neurodegeneration from the very early stages of PD. Moreover, its brain structural correlates and its lack of relationship with dopaminergic depletion or amyloidosis suggests that NfL could track the underlying pathological process leading to PD dementia. Parkinson's disease Biomarkers Cognitive decline NfL Cortical thinning Pérez-González, Rocío verfasserin aut Martínez-Horta, Saul verfasserin aut Marín-Lahoz, Juan verfasserin aut Pagonabarraga, Javier verfasserin aut Kulisevsky, Jaime verfasserin aut Enthalten in Parkinsonism & related disorders Amsterdam [u.a.] : Elsevier Science, 1995 74, Seite 43-49 Online-Ressource (DE-627)32448898X (DE-600)2027635-7 (DE-576)272349704 1873-5126 nnns volume:74 pages:43-49 GBV_USEFLAG_U SYSFLAG_U GBV_ELV GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.90 Neurologie AR 74 43-49
allfieldsGer	10.1016/j.parkreldis.2020.04.009 doi (DE-627)ELV004288823 (ELSEVIER)S1353-8020(20)30104-8 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl Sampedro, Frederic verfasserin aut Serum neurofilament light chain levels reflect cortical neurodegeneration in de novo Parkinson's disease 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction: Cognitive impairment and dementia are highly prevalent non-motor complications in Parkinson's disease (PD) with deleterious consequences for patients and caregivers. With no treatment currently available, finding and validating minimally-invasive biomarkers of neurodegeneration in this population represents an urgent need for clinical trials targeting its prevention or delay. Recently, serum neurofilament light chain (NfL) levels have been identified as a promising biomarker of neural loss, but whether they reflect cortical neurodegeneration in early PD stages has not been addressed.Methods: From the Parkinson's Progression Markers Initiative (PPMI), we selected 133 de novo PD patients and 56 healthy controls (HC) with available structural neuroimaging and serum NfL data. We then studied whether NfL levels were abnormal in the PD group with respect to HC, and whether they correlated with cognitive indicators and cortical macro (cortical thinning) and microstructural (increased intracortical mean diffusivity) degeneration.Results: Serum NfL levels were significantly increased in the PD group (p = 0.010), and were also related to worse cognitive performance and a cortical macro and microstructural compromise (p < 0.05 corrected). These associations were observed both cross-sectionally and longitudinally within a one-year follow-up period. Topographically, NfL levels reflected posterior-cortical deterioration rather than frontal damage. Importantly, NfL levels were not associated with striatal SPECT-DAT uptake or β-amyloid burden.Discussion: Our results show that serum NfL levels reflect cortical neurodegeneration from the very early stages of PD. Moreover, its brain structural correlates and its lack of relationship with dopaminergic depletion or amyloidosis suggests that NfL could track the underlying pathological process leading to PD dementia. Parkinson's disease Biomarkers Cognitive decline NfL Cortical thinning Pérez-González, Rocío verfasserin aut Martínez-Horta, Saul verfasserin aut Marín-Lahoz, Juan verfasserin aut Pagonabarraga, Javier verfasserin aut Kulisevsky, Jaime verfasserin aut Enthalten in Parkinsonism & related disorders Amsterdam [u.a.] : Elsevier Science, 1995 74, Seite 43-49 Online-Ressource (DE-627)32448898X (DE-600)2027635-7 (DE-576)272349704 1873-5126 nnns volume:74 pages:43-49 GBV_USEFLAG_U SYSFLAG_U GBV_ELV GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.90 Neurologie AR 74 43-49
allfieldsSound	10.1016/j.parkreldis.2020.04.009 doi (DE-627)ELV004288823 (ELSEVIER)S1353-8020(20)30104-8 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl Sampedro, Frederic verfasserin aut Serum neurofilament light chain levels reflect cortical neurodegeneration in de novo Parkinson's disease 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction: Cognitive impairment and dementia are highly prevalent non-motor complications in Parkinson's disease (PD) with deleterious consequences for patients and caregivers. With no treatment currently available, finding and validating minimally-invasive biomarkers of neurodegeneration in this population represents an urgent need for clinical trials targeting its prevention or delay. Recently, serum neurofilament light chain (NfL) levels have been identified as a promising biomarker of neural loss, but whether they reflect cortical neurodegeneration in early PD stages has not been addressed.Methods: From the Parkinson's Progression Markers Initiative (PPMI), we selected 133 de novo PD patients and 56 healthy controls (HC) with available structural neuroimaging and serum NfL data. We then studied whether NfL levels were abnormal in the PD group with respect to HC, and whether they correlated with cognitive indicators and cortical macro (cortical thinning) and microstructural (increased intracortical mean diffusivity) degeneration.Results: Serum NfL levels were significantly increased in the PD group (p = 0.010), and were also related to worse cognitive performance and a cortical macro and microstructural compromise (p < 0.05 corrected). These associations were observed both cross-sectionally and longitudinally within a one-year follow-up period. Topographically, NfL levels reflected posterior-cortical deterioration rather than frontal damage. Importantly, NfL levels were not associated with striatal SPECT-DAT uptake or β-amyloid burden.Discussion: Our results show that serum NfL levels reflect cortical neurodegeneration from the very early stages of PD. Moreover, its brain structural correlates and its lack of relationship with dopaminergic depletion or amyloidosis suggests that NfL could track the underlying pathological process leading to PD dementia. Parkinson's disease Biomarkers Cognitive decline NfL Cortical thinning Pérez-González, Rocío verfasserin aut Martínez-Horta, Saul verfasserin aut Marín-Lahoz, Juan verfasserin aut Pagonabarraga, Javier verfasserin aut Kulisevsky, Jaime verfasserin aut Enthalten in Parkinsonism & related disorders Amsterdam [u.a.] : Elsevier Science, 1995 74, Seite 43-49 Online-Ressource (DE-627)32448898X (DE-600)2027635-7 (DE-576)272349704 1873-5126 nnns volume:74 pages:43-49 GBV_USEFLAG_U SYSFLAG_U GBV_ELV GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.90 Neurologie AR 74 43-49
language	English
source	Enthalten in Parkinsonism & related disorders 74, Seite 43-49 volume:74 pages:43-49
sourceStr	Enthalten in Parkinsonism & related disorders 74, Seite 43-49 volume:74 pages:43-49
format_phy_str_mv	Article
bklname	Neurologie
institution	findex.gbv.de
topic_facet	Parkinson's disease Biomarkers Cognitive decline NfL Cortical thinning
dewey-raw	610
isfreeaccess_bool	false
container_title	Parkinsonism & related disorders
authorswithroles_txt_mv	Sampedro, Frederic @@aut@@ Pérez-González, Rocío @@aut@@ Martínez-Horta, Saul @@aut@@ Marín-Lahoz, Juan @@aut@@ Pagonabarraga, Javier @@aut@@ Kulisevsky, Jaime @@aut@@
publishDateDaySort_date	2020-01-01T00:00:00Z
hierarchy_top_id	32448898X
dewey-sort	3610
id	ELV004288823
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV004288823</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230524144107.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230502s2020 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.parkreldis.2020.04.009</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV004288823</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S1353-8020(20)30104-8</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rda</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.90</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Sampedro, Frederic</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Serum neurofilament light chain levels reflect cortical neurodegeneration in de novo Parkinson's disease</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2020</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Introduction: Cognitive impairment and dementia are highly prevalent non-motor complications in Parkinson's disease (PD) with deleterious consequences for patients and caregivers. 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We then studied whether NfL levels were abnormal in the PD group with respect to HC, and whether they correlated with cognitive indicators and cortical macro (cortical thinning) and microstructural (increased intracortical mean diffusivity) degeneration.Results: Serum NfL levels were significantly increased in the PD group (p = 0.010), and were also related to worse cognitive performance and a cortical macro and microstructural compromise (p < 0.05 corrected). These associations were observed both cross-sectionally and longitudinally within a one-year follow-up period. Topographically, NfL levels reflected posterior-cortical deterioration rather than frontal damage. Importantly, NfL levels were not associated with striatal SPECT-DAT uptake or β-amyloid burden.Discussion: Our results show that serum NfL levels reflect cortical neurodegeneration from the very early stages of PD. 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author	Sampedro, Frederic
spellingShingle	Sampedro, Frederic ddc 610 bkl 44.90 misc Parkinson's disease misc Biomarkers misc Cognitive decline misc NfL misc Cortical thinning Serum neurofilament light chain levels reflect cortical neurodegeneration in de novo Parkinson's disease
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topic_title	610 DE-600 44.90 bkl Serum neurofilament light chain levels reflect cortical neurodegeneration in de novo Parkinson's disease Parkinson's disease Biomarkers Cognitive decline NfL Cortical thinning
topic	ddc 610 bkl 44.90 misc Parkinson's disease misc Biomarkers misc Cognitive decline misc NfL misc Cortical thinning
topic_unstemmed	ddc 610 bkl 44.90 misc Parkinson's disease misc Biomarkers misc Cognitive decline misc NfL misc Cortical thinning
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title	Serum neurofilament light chain levels reflect cortical neurodegeneration in de novo Parkinson's disease
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title_full	Serum neurofilament light chain levels reflect cortical neurodegeneration in de novo Parkinson's disease
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author_browse	Sampedro, Frederic Pérez-González, Rocío Martínez-Horta, Saul Marín-Lahoz, Juan Pagonabarraga, Javier Kulisevsky, Jaime
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title_sort	serum neurofilament light chain levels reflect cortical neurodegeneration in de novo parkinson's disease
title_auth	Serum neurofilament light chain levels reflect cortical neurodegeneration in de novo Parkinson's disease
abstract	Introduction: Cognitive impairment and dementia are highly prevalent non-motor complications in Parkinson's disease (PD) with deleterious consequences for patients and caregivers. With no treatment currently available, finding and validating minimally-invasive biomarkers of neurodegeneration in this population represents an urgent need for clinical trials targeting its prevention or delay. Recently, serum neurofilament light chain (NfL) levels have been identified as a promising biomarker of neural loss, but whether they reflect cortical neurodegeneration in early PD stages has not been addressed.Methods: From the Parkinson's Progression Markers Initiative (PPMI), we selected 133 de novo PD patients and 56 healthy controls (HC) with available structural neuroimaging and serum NfL data. We then studied whether NfL levels were abnormal in the PD group with respect to HC, and whether they correlated with cognitive indicators and cortical macro (cortical thinning) and microstructural (increased intracortical mean diffusivity) degeneration.Results: Serum NfL levels were significantly increased in the PD group (p = 0.010), and were also related to worse cognitive performance and a cortical macro and microstructural compromise (p < 0.05 corrected). These associations were observed both cross-sectionally and longitudinally within a one-year follow-up period. Topographically, NfL levels reflected posterior-cortical deterioration rather than frontal damage. Importantly, NfL levels were not associated with striatal SPECT-DAT uptake or β-amyloid burden.Discussion: Our results show that serum NfL levels reflect cortical neurodegeneration from the very early stages of PD. Moreover, its brain structural correlates and its lack of relationship with dopaminergic depletion or amyloidosis suggests that NfL could track the underlying pathological process leading to PD dementia.
abstractGer	Introduction: Cognitive impairment and dementia are highly prevalent non-motor complications in Parkinson's disease (PD) with deleterious consequences for patients and caregivers. With no treatment currently available, finding and validating minimally-invasive biomarkers of neurodegeneration in this population represents an urgent need for clinical trials targeting its prevention or delay. Recently, serum neurofilament light chain (NfL) levels have been identified as a promising biomarker of neural loss, but whether they reflect cortical neurodegeneration in early PD stages has not been addressed.Methods: From the Parkinson's Progression Markers Initiative (PPMI), we selected 133 de novo PD patients and 56 healthy controls (HC) with available structural neuroimaging and serum NfL data. We then studied whether NfL levels were abnormal in the PD group with respect to HC, and whether they correlated with cognitive indicators and cortical macro (cortical thinning) and microstructural (increased intracortical mean diffusivity) degeneration.Results: Serum NfL levels were significantly increased in the PD group (p = 0.010), and were also related to worse cognitive performance and a cortical macro and microstructural compromise (p < 0.05 corrected). These associations were observed both cross-sectionally and longitudinally within a one-year follow-up period. Topographically, NfL levels reflected posterior-cortical deterioration rather than frontal damage. Importantly, NfL levels were not associated with striatal SPECT-DAT uptake or β-amyloid burden.Discussion: Our results show that serum NfL levels reflect cortical neurodegeneration from the very early stages of PD. Moreover, its brain structural correlates and its lack of relationship with dopaminergic depletion or amyloidosis suggests that NfL could track the underlying pathological process leading to PD dementia.
abstract_unstemmed	Introduction: Cognitive impairment and dementia are highly prevalent non-motor complications in Parkinson's disease (PD) with deleterious consequences for patients and caregivers. With no treatment currently available, finding and validating minimally-invasive biomarkers of neurodegeneration in this population represents an urgent need for clinical trials targeting its prevention or delay. Recently, serum neurofilament light chain (NfL) levels have been identified as a promising biomarker of neural loss, but whether they reflect cortical neurodegeneration in early PD stages has not been addressed.Methods: From the Parkinson's Progression Markers Initiative (PPMI), we selected 133 de novo PD patients and 56 healthy controls (HC) with available structural neuroimaging and serum NfL data. We then studied whether NfL levels were abnormal in the PD group with respect to HC, and whether they correlated with cognitive indicators and cortical macro (cortical thinning) and microstructural (increased intracortical mean diffusivity) degeneration.Results: Serum NfL levels were significantly increased in the PD group (p = 0.010), and were also related to worse cognitive performance and a cortical macro and microstructural compromise (p < 0.05 corrected). These associations were observed both cross-sectionally and longitudinally within a one-year follow-up period. Topographically, NfL levels reflected posterior-cortical deterioration rather than frontal damage. Importantly, NfL levels were not associated with striatal SPECT-DAT uptake or β-amyloid burden.Discussion: Our results show that serum NfL levels reflect cortical neurodegeneration from the very early stages of PD. Moreover, its brain structural correlates and its lack of relationship with dopaminergic depletion or amyloidosis suggests that NfL could track the underlying pathological process leading to PD dementia.
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title_short	Serum neurofilament light chain levels reflect cortical neurodegeneration in de novo Parkinson's disease
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author2	Pérez-González, Rocío Martínez-Horta, Saul Marín-Lahoz, Juan Pagonabarraga, Javier Kulisevsky, Jaime
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doi_str	10.1016/j.parkreldis.2020.04.009
up_date	2024-07-06T22:29:26.562Z
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We then studied whether NfL levels were abnormal in the PD group with respect to HC, and whether they correlated with cognitive indicators and cortical macro (cortical thinning) and microstructural (increased intracortical mean diffusivity) degeneration.Results: Serum NfL levels were significantly increased in the PD group (p = 0.010), and were also related to worse cognitive performance and a cortical macro and microstructural compromise (p < 0.05 corrected). These associations were observed both cross-sectionally and longitudinally within a one-year follow-up period. Topographically, NfL levels reflected posterior-cortical deterioration rather than frontal damage. Importantly, NfL levels were not associated with striatal SPECT-DAT uptake or β-amyloid burden.Discussion: Our results show that serum NfL levels reflect cortical neurodegeneration from the very early stages of PD. 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Serum neurofilament light chain levels reflect cortical neurodegeneration in de novo Parkinson's disease

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