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Cognitive impairment in Glucocerebrosidase (GBA)-associated PD: Not primarily associated with cerebrospinal fluid Abeta and Tau profiles.
Mov Disord 2017; 32(12):1780-1783MD

Abstract

BACKGROUND

A proportion of idiopathic Parkinson's disease patients (PDidiopathic) with dementia show altered CSF profiles of amyloid β (Aβ) and Tau. PD patients with Glucocerebrosidase (GBA) mutations (PDGBA) present with even more cognitive decline than seen in PDidiopathic .

OBJECTIVE

The objective of this study was to evaluate whether CSF profiles of Aβ and tau are associated with the prominent cognitive impairment in PDGBA .

METHODS

CSF levels of Aβ1-42 , t-Tau, p-Tau, and total alpha-synuclein were assessed in 479 participants (50 PDGBA , 308 PDidiopathic , 121 healthy controls).

RESULTS

Older age was associated with cognitive impairment in PDGBA and PDidiopathic . Despite prominent cognitive impairment, PDGBA showed similar CSF levels of Aβ1-42 , t-Tau, and p-Tau as seen in healthy controls. In contrast, lower levels of Aβ1-42 and higher levels of t-Tau and p-Tau were associated with worse cognitive performance in PDidiopathic .

CONCLUSIONS

The prominent cognitive impairment in PDGBA seems not primarily associated with Aβ and Tau profiles in CSF. © 2017 International Parkinson and Movement Disorder Society.

Authors+Show Affiliations

Center of Neurology, Department of Neurodegeneration and Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany. German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.Center of Neurology, Department of Neurodegeneration and Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany. German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.Center of Neurology, Department of Neurodegeneration and Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany. German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.Center of Neurology, Department of Neurodegeneration and Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany. Neurology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy.Center of Neurology, Department of Neurodegeneration and Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany. German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.Center of Neurology, Department of Neurodegeneration and Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany. German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.Center of Neurology, Department of Neurodegeneration and Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany.Center of Neurology, Department of Neurodegeneration and Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany. German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.Gertrudis Klinik, Parkinson-Center, Leun-Biskirchen, Germany.AJ Roboscreen GmbH, Leipzig, Germany.Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK.Center of Neurology, Department of Neurodegeneration and Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany. German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.Center of Neurology, Department of Neurodegeneration and Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany. German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.Center of Neurology, Department of Neurodegeneration and Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany. German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany. Department of Neurology, Christian-Albrechts University, Kiel, Germany.Center of Neurology, Department of Neurodegeneration and Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany. German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany. Department of Neurology, Christian-Albrechts University, Kiel, Germany.Center of Neurology, Department of Neurodegeneration and Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany. German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

29094781

Citation

Lerche, Stefanie, et al. "Cognitive Impairment in Glucocerebrosidase (GBA)-associated PD: Not Primarily Associated With Cerebrospinal Fluid Abeta and Tau Profiles." Movement Disorders : Official Journal of the Movement Disorder Society, vol. 32, no. 12, 2017, pp. 1780-1783.
Lerche S, Schulte C, Srulijes K, et al. Cognitive impairment in Glucocerebrosidase (GBA)-associated PD: Not primarily associated with cerebrospinal fluid Abeta and Tau profiles. Mov Disord. 2017;32(12):1780-1783.
Lerche, S., Schulte, C., Srulijes, K., Pilotto, A., Rattay, T. W., Hauser, A. K., ... Brockmann, K. (2017). Cognitive impairment in Glucocerebrosidase (GBA)-associated PD: Not primarily associated with cerebrospinal fluid Abeta and Tau profiles. Movement Disorders : Official Journal of the Movement Disorder Society, 32(12), pp. 1780-1783. doi:10.1002/mds.27199.
Lerche S, et al. Cognitive Impairment in Glucocerebrosidase (GBA)-associated PD: Not Primarily Associated With Cerebrospinal Fluid Abeta and Tau Profiles. Mov Disord. 2017;32(12):1780-1783. PubMed PMID: 29094781.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cognitive impairment in Glucocerebrosidase (GBA)-associated PD: Not primarily associated with cerebrospinal fluid Abeta and Tau profiles. AU - Lerche,Stefanie, AU - Schulte,Claudia, AU - Srulijes,Karin, AU - Pilotto,Andrea, AU - Rattay,Tim W, AU - Hauser,Ann-Kathrin, AU - Stransky,Elke, AU - Deuschle,Christian, AU - Csoti,Ilona, AU - Lachmann,Ingolf, AU - Zetterberg,Henrik, AU - Liepelt-Scarfone,Inga, AU - Gasser,Thomas, AU - Maetzler,Walter, AU - Berg,Daniela, AU - Brockmann,Kathrin, Y1 - 2017/11/02/ PY - 2017/07/05/received PY - 2017/08/15/revised PY - 2017/09/06/accepted PY - 2017/11/3/pubmed PY - 2018/7/20/medline PY - 2017/11/3/entrez KW - Abeta KW - CSF KW - GBA KW - Parkinson KW - Tau KW - alpha-synuclein SP - 1780 EP - 1783 JF - Movement disorders : official journal of the Movement Disorder Society JO - Mov. Disord. VL - 32 IS - 12 N2 - BACKGROUND: A proportion of idiopathic Parkinson's disease patients (PDidiopathic) with dementia show altered CSF profiles of amyloid β (Aβ) and Tau. PD patients with Glucocerebrosidase (GBA) mutations (PDGBA) present with even more cognitive decline than seen in PDidiopathic . OBJECTIVE: The objective of this study was to evaluate whether CSF profiles of Aβ and tau are associated with the prominent cognitive impairment in PDGBA . METHODS: CSF levels of Aβ1-42 , t-Tau, p-Tau, and total alpha-synuclein were assessed in 479 participants (50 PDGBA , 308 PDidiopathic , 121 healthy controls). RESULTS: Older age was associated with cognitive impairment in PDGBA and PDidiopathic . Despite prominent cognitive impairment, PDGBA showed similar CSF levels of Aβ1-42 , t-Tau, and p-Tau as seen in healthy controls. In contrast, lower levels of Aβ1-42 and higher levels of t-Tau and p-Tau were associated with worse cognitive performance in PDidiopathic . CONCLUSIONS: The prominent cognitive impairment in PDGBA seems not primarily associated with Aβ and Tau profiles in CSF. © 2017 International Parkinson and Movement Disorder Society. SN - 1531-8257 UR - https://www.unboundmedicine.com/medline/citation/29094781/Cognitive_impairment_in_Glucocerebrosidase__GBA__associated_PD:_Not_primarily_associated_with_cerebrospinal_fluid_Abeta_and_Tau_profiles_ L2 - https://doi.org/10.1002/mds.27199 DB - PRIME DP - Unbound Medicine ER -