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

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

2010 November 15; 25(15): 2682–2685 | Thomas J. Montine, Min Shi, Joseph F. Quinn, Elaine R. Peskind, Suzanne Craft, Carmen Ginghina, Kathryn A. Chung, Hojoong Kim, Douglas R. Galasko, Joseph Jankovic, Cyrus P. Zabetian, James B. Leverenz, and Jing Zhang
This study aimed to investigate whether the cerebrospinal fluid (CSF) biomarker signature associated with Alzheimer's disease (AD) is present in a subset of individuals with Parkinson's disease (PD) and cognitive impairment. The researchers quantified CSF Aβ42, total tau (T-tau), and phospho-tau (P181-Tau) in 345 individuals across seven groups: controls ≤ 50 years, controls > 50 years, amnestic Mild Cognitive Impairment (aMCI), AD, PD, PD-CIND, and PD-D. They observed expected changes in AD and aMCI compared to age-matched or younger controls. CSF Aβ42 was reduced in PD-CIND and PD-D, while 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, suggesting that abnormal metabolism of Aβ42 may be a common feature of PD-CIND and PD-D. The study highlights the potential of CSF biomarkers in identifying patients with PD and co-morbid AD, though it also indicates that this is a minority of patients. Further research is needed to explore other causes of cognitive impairment and dementia in PD.This study aimed to investigate whether the cerebrospinal fluid (CSF) biomarker signature associated with Alzheimer's disease (AD) is present in a subset of individuals with Parkinson's disease (PD) and cognitive impairment. The researchers quantified CSF Aβ42, total tau (T-tau), and phospho-tau (P181-Tau) in 345 individuals across seven groups: controls ≤ 50 years, controls > 50 years, amnestic Mild Cognitive Impairment (aMCI), AD, PD, PD-CIND, and PD-D. They observed expected changes in AD and aMCI compared to age-matched or younger controls. CSF Aβ42 was reduced in PD-CIND and PD-D, while 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, suggesting that abnormal metabolism of Aβ42 may be a common feature of PD-CIND and PD-D. The study highlights the potential of CSF biomarkers in identifying patients with PD and co-morbid AD, though it also indicates that this is a minority of patients. Further research is needed to explore other causes of cognitive impairment and dementia in PD.
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