CSF Aβ42 and tau in Parkinson's disease with cognitive impairment

Movement Disorders - Tập 25 Số 15 - Trang 2682-2685 - 2010
Thomas J. Montine1,2, Min Shi1,2, Joseph F. Quinn3, Elaine R. Peskind4,5, Suzanne Craft4,6, Carmen Ginghină1, Kathryn A. Chung3, Hojoong Kim7,6, Douglas Galasko8, Joseph Jankovic9, Cyrus P. Zabetian7,6, James B. Leverenz7,5, Jing Zhang1
1Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA
2Thomas J. Montine and Min Shi contributed equally to this work.
3Department of Neurology, Oregon Health & Science University, Portland, Oregon, USA
4Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, Washington, USA
5VA Northwest Network Mental Illness Research, Education and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA
6Geriatric Research Education and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA
7Department of Neurology, University of Washington School of Medicine Seattle Washington, USA
8Department of Neurosciences, University of California at San Diego, San Diego, California, USA
9Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology Baylor College of Medicine Houston Texas USA

Tóm tắt

Abstract

We tested the hypothesis that the CSF biomarker signature associated with Alzheimer's disease (AD) is present in a subset of individuals with Parkinson's disease and Dementia (PD‐D) or with PD and Cognitive Impairment, Not Dementia (PD‐CIND). We quantified CSF Aβ42, total tau (T‐tau), and phospho‐tau (P181‐tau) using commercially available kits. Samples were from 345 individuals in seven groups (n): Controls ≤50 years (35), Controls >50 years (115), amnestic Mild Cognitive Impairment (aMCI) (24), AD (49), PD (49), PD‐CIND (62), and PD‐D (11). We observed expected changes in AD or aMCI compared with age‐matched or younger controls. CSF Aβ42 was reduced in PD‐CIND (P < 0.05) and PD‐D (P < 0.01), whereas average CSF T‐tau and P181‐tau were unchanged or decreased. One‐third of PD‐CIND and one‐half of PD‐D patients had the biomarker signature of AD. Abnormal metabolism of Aβ42 may be a common feature of PD‐CIND and PD‐D. © 2010 Movement Disorder Society

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