Background: Small vessel disease and white matter hyperintensities (WMH) as its surrogate marker are known to predict cognitive decline in the elderly. However, the influence of vascular lesions on cognitive impairment in Parkinson's disease (PD) has been discussed controversial so far. The Aim of this study was to evaluate the predictive role of volume and location of white matter hyperintensities (WMH) on cognitive decline in de novo PD patients.
Methods: 108 diagnosed drug-naïve PD patients (64 ± 9 years, 38% women) from the DeNoPa Cohort underwent extensive neuropsychological testing with re-testing in 24-month later. Movement Disorder Society criteria for the classification of mild cognitive impairment (MCI) and dementia in PD were applied. Participants that declined from normal cognition or MCI at baseline to MCI or dementia at 24-month follow-up (FU) or from MCI to dementia at 24-month FU were defined as "converters". Subjects with stable cognitive level or improved cognitive status were classified as "non-converters". Magnetic resonance imaging (MRI) was performed, and the extent of WMH was assessed as global volume and as WMH load within cholinergic pathways using the Cholinergic Pathways Hyperintensities Scale. We compared Parkinson's disease subjects with age-matched, neurologically healthy controls.
Results: At total of 29 (27%) patients met the criteria for MCI at baseline, whereas 79 (73%) patients had no cognitive impairment. During the 24-month FU 33 patients showed cognitive decline ("converter") compared to 75 "non-converters". Multivariable logistic regression revealed no significant differences between "cognitively impaired" and "cognitively non-impaired" patients and participants of the control group at baseline or between "converter" and "non-converter" regarding the extent of WMH globally or within cholinergic pathways.
Conclusions: We could not identify global or localized WMH load as predictive markers of cognitive decline in de novo PD patients indicating that cerebral small vessel disease is not a critical modifier of cognitive function in early PD.
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