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Editorial commentary
Novel evidence associates higher plasma α-synuclein levels and cognitive impairment in Parkinson’s disease
  1. Dag Aarsland1,2,
  2. Anto P Rajkumar1,2,
  3. Abdul Hye1,3
  1. 1Department of Old Age Psychiatry, Institute of Psychiatry, Psychology, & Neuroscience, King’s College London, London, UK
  2. 2Mental Health of Older Adults and Dementia Clinical Academic Group, South London and Maudsley NHS Foundation Trust, London, UK
  3. 3NIHR Biomedical Research Centre for Mental Health and Biomedical Research Unit for Dementia at South London and Maudsley NHS Foundation trust, London, UK
  1. Correspondence to Professor Dag Aarsland, Department of Old Age Psychiatry, Institute of Psychiatry, Psychology, & Neuroscience, King’s College London, 16, De Crespigny Park, London SE5 8AF, UK; dag.aarsland{at}kcl.ac.uk

https://doi.org/10.1136/jnnp-2017-315821

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    A new and highly sensitive blood test of α-synuclein confirms that associated with cognitive impairment in Parkinson’s disease

    Cognitive impairment is common in Parkinson’s disease (PD) and is linked to cortical alpha-synuclein (α-syn) pathology. Biomarkers predicting time and rate of cognitive decline in PD are needed.1 Levels of total, oligomeric, and phosphorylated α-syn in peripheral tissues and body fluids of people with PD have been extensively evaluated.2 Most studies have used cerebrospinal fluid (CSF), but findings have been disappointing. A recent meta-analysis that included 17 studies (n=3311) reported significantly lower levels of CSF α-syn in PD, compared with healthy or neurological controls, but concluded that CSF α-syn levels alone are not sufficient for diagnosing PD early.3 4 Factors leading to variation among studies include different technical platforms and antibody variability. An additional complicating factor is the …

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    Footnotes

    • Contributors All three authors contributed to the writing of this commentary.

    • Competing interests DA has received research support and/or honoraria from Astra-Zeneca, H. Lundbeck, Novartis Pharmaceuticals and GE Health, and serves as paid consultant for H. Lundbeck, Eisai and Axovant. DA is a Royal Society Wolfson Research Merit Award Holder and would like to thank the Wolfson Foundation and the Royal Society for their support. This paper represents independent research partly funded by the National Institute for Health Research (NIHR) Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King’s College London. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health.

    • Provenance and peer review Commissioned; internally peer reviewed.

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