02:44pm Tuesday 25 July 2017

Researchers Identify Biomarker for Early Cognitive Decline in Parkinson’s Disease Patients

Many patients with Parkinson’s Disease (PD) develop mild cognitive impairment (MCI) or dementia. Identifying biomarkers for cognitive impairment could be instrumental in facilitating both early diagnosis of MCI and developing new cognitive-enhancing treatments. New research published in the Journal of Parkinson’s Disease indicates that lower concentrations of α-synuclein in cerebrospinal fluid (CSF) is associated with reduced performance on several cognitive tests.

“This is the largest study exploring the association between CSF biomarkers and cognition in PD, and one of few to explore if α-synuclein is associated with cognitive impairment,” explained lead investigator Ragnhild E. Skogseth, MD, of Haraldsplass Deaconess Hospital and the Department of Clinical Medicine, University of Bergen (Norway).

CSF markers beta-amyloid42 (abeta42), total tau protein (t-tau), phosphorylated tau protein (p-tau), and α-synuclein reflect pathophysiological changes relevant to cognition in PD. If changes in these biomarkers can predict cognitive decline, patients could be informed to seek possible treatments.

Part of the Parkinson’s Progression Markers Initiative (PPMI), an international project focusing on development of biomarkers of progression in PD, this study was comprised of 414 patients with untreated PD without dementia and 196 health control (HC) subjects from 24 clinical sites worldwide. The patients were evaluated for multiple cognitive skills, including visuospatial functions, verbal memory, executive function, and attention. Patients were defined as having MCI (PD-MCI) if they showed impairment on two or more tests, while patients not fulfilling criteria for MCI were classified as having normal cognition (PD-NC). The Unified Parkinson’s Disease Rating Score (UPDRS) was used to evaluate the progression of the disease in the PD patients.

The investigation determined that lower α-synuclein was associated with reduced performance in cognition testing in the whole PD-group. Abeta42 was significantly decreased in PD with mild cognitive impairment compared with controls, while values in PD without MCI were identical to the HC group controls.

After analyzing demographics and the results of CSF analysis, there were no significant differences in gender, age, or education between PD and HC patients. Among the PD patients, 140 PD-MCI subjects were significantly older, had less formal education, and had higher UPDRS scores than the 274 PD-NC subjects.

“The association between reduced CSF α-synuclein concentrations and cognition suggests that α-synuclein pathology contributes to early cognitive impairment in PD, in particular to executive-attentional dysfunction. Longitudinal analyses are needed to determine if this and other CSF biomarkers in early Parkinson’s disease are associated with the risk of future cognitive decline and dementia,” noted Dr. Skogseth.

“This is a very important study that not only gives insight into the mechanisms that might underlie cognitive decline in Parkinson’s disease, but it might also represent the first steps in the development of a much needed biomarker that can predict which patients will develop dementia,” commented Patrik Brundin, MD, PhD, Editor-in-Chief of the Journal of Parkinson’s Disease and Director of the Center for Neurodegenerative Science at Van Andel Research Institute in Grand Rapids, MI.

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NOTES FOR EDITORS

Associations between Cerebrospinal Fluid Biomarkers and Cognition in Early Untreated Parkinson’s Disease,” by Ragnhild E. Skogseth, MD; Kolbjorn Bronnick, PhD; Joana B. Pereira, PhD; Brit Mollenhauer, MD, PhD; Daniel Weintraub, MD, PhD; Tormod Fladby, MD, PhD; and Dag Aarsland, MD, PhD (DOI 10.3233/JPD-150682), Journal of Parkinson’s Disease, Volume 5, Issue 4, published by IOS Press.

To obtain the full text of this study and additional information contact Daphne Watrin, IOS Press, at +31 20 688 3355, d.watrin@iospress.nl. Journalists wishing to interview the authors should contact Ragnhild E. Skogseth, MD, at +47 99 29 81 71; ragnhild.skogseth@gmail.com or Ida Kristine Sangnes at +47 95 78 78 76 or ida.kristine.sangnes@haraldsplass.no.

ABOUT THE JOURNAL OF PARKINSON’S DISEASE (JPD)

Launched in 2011 the Journal of Parkinson’s Disease is dedicated to providing an open forum for original research in basic science, translational research and clinical medicine that will expedite our fundamental understanding and improve treatment of Parkinson’s disease. The journal is international and multidisciplinary and aims to promote progress in the epidemiology, etiology, genetics, molecular correlates, pathogenesis, pharmacology, psychology, diagnosis and treatment of Parkinson’s disease. It publishes research reports, reviews, short communications, and letters-to-the-editor and offers very rapid publication and an affordable open access option. 

ABOUT IOS PRESS

Commencing its publishing activities in 1987, IOS Press serves the information needs of scientific and medical communities worldwide. IOS Press now (co-)publishes over 100 international journals and about 75 book titles each year on subjects ranging from computer sciences and mathematics to medicine and the natural sciences.

IOS Press continues its rapid growth, embracing new technologies for the timely dissemination of information. All journals are available electronically and an e-book platform was launched in 2005.

Headquartered in Amsterdam with satellite offices in the USA, Germany, India and China, IOS Press has established several strategic co-publishing initiatives. Notable acquisitions included Delft University Press in 2005 and Millpress Science Publishers in 2008.


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