2010 November 15 | Thomas J. Montine¹,†, Min Shi¹,†, Joseph F. Quinn², Elaine R. Peskind³,⁴, Suzanne Craft³,⁵, Carmen Ginghina¹, Kathryn A. Chung², Hojoong Kim⁵,⁸, Douglas R. Galasko⁶, Joseph Jankovic⁷, Cyrus P. Zabetian⁵,⁸, James B. Leverenz⁴,⁸, and Jing Zhang¹
This study investigated the presence of Alzheimer's disease (AD) biomarkers in individuals with Parkinson's disease (PD) and cognitive impairment. CSF levels of Aβ42, total tau (T-tau), and phosphorylated tau (P181-tau) were measured in 345 individuals across seven groups, including controls, amnestic mild cognitive impairment (aMCI), AD, PD, PD-CIND, and PD-D. The results showed that PD-CIND and PD-D patients had reduced CSF Aβ42 levels compared to controls, while T-tau and P181-tau levels were unchanged or decreased. One-third of PD-CIND and half of PD-D patients exhibited AD-like biomarker profiles. These findings suggest that abnormal Aβ42 metabolism may be a common feature of PD-CIND and PD-D. The study highlights the importance of identifying patients with PD and co-morbid AD to guide clinical trials and patient management. The results also indicate that AD is not a common comorbidity in PD with cognitive impairment, suggesting that other causes may be more prevalent. The study used validated CSF biomarkers to assess AD-related processes in PD patients, providing insights into the potential overlap between PD and AD. The findings underscore the need for further research into common causes of cognitive impairment and dementia in PD patients.This study investigated the presence of Alzheimer's disease (AD) biomarkers in individuals with Parkinson's disease (PD) and cognitive impairment. CSF levels of Aβ42, total tau (T-tau), and phosphorylated tau (P181-tau) were measured in 345 individuals across seven groups, including controls, amnestic mild cognitive impairment (aMCI), AD, PD, PD-CIND, and PD-D. The results showed that PD-CIND and PD-D patients had reduced CSF Aβ42 levels compared to controls, while T-tau and P181-tau levels were unchanged or decreased. One-third of PD-CIND and half of PD-D patients exhibited AD-like biomarker profiles. These findings suggest that abnormal Aβ42 metabolism may be a common feature of PD-CIND and PD-D. The study highlights the importance of identifying patients with PD and co-morbid AD to guide clinical trials and patient management. The results also indicate that AD is not a common comorbidity in PD with cognitive impairment, suggesting that other causes may be more prevalent. The study used validated CSF biomarkers to assess AD-related processes in PD patients, providing insights into the potential overlap between PD and AD. The findings underscore the need for further research into common causes of cognitive impairment and dementia in PD patients.