Abstract
Cognition is often affected early in Parkinson’s disease (PD). Lewy body and amyloid β (Aβ) pathology and cortical atrophy may be involved. The aim of this study was to examine whether medial temporal lobe structural changes may be linked to cerebrospinal fluid (CSF) biomarker levels and cognition in early PD. PD patients had smaller volumes of total hippocampus, presubiculum, subiculum, CA2–3, CA4-DG, and hippocampal tail compared with normal controls (NCs). In the PD group, lower CSF Aβ38 and 42 were significant predictors for thinner perirhinal cortex. Lower Aβ42 and smaller presubiculum and subiculum predicted poorer verbal learning and delayed verbal recall. Smaller total hippocampus, presubiculum and subiculum predicted poorer visuospatial copying. Lower Aβ38 and 40 and thinner perirhinal cortex predicted poorer delayed visual reproduction. In conclusion, smaller volumes of hippocampal subfields and subhippocampal cortex thickness linked to lower CSF Aβ levels may contribute to cognitive impairment in early PD. Thirty-three early PD patients (13 without, 5 with subjective, and 15 with mild cognitive impairment) and NC had 3 T magnetic resonance imaging (MRI) scans. The MRI scans were post processed for volumes of hippocampal subfields and entorhinal and perirhinal cortical thickness. Lumbar puncture for CSF biomarkers Aβ38, 40, 42, total tau, phosphorylated tau (Innogenetics), and total α-synuclein (Meso Scale Diagnostics) were performed. Multiple regression analyses were used for between-group comparisons of the MRI measurements in the NC and PD groups and for assessment of CSF biomarkers and neuropsychological tests in relation to morphometry in the PD group.
Highlights
Cognitive impairment (CI) is a common non-motor feature in Parkinson’s disease (PD)
The PD patients were in early stages with mild to moderate motor symptoms, 13 cases had normal cognition, 5 had subjective CI (SCI), and 15 had mild CI (MCI), and all had Aβ42 levels above in-house diagnostic cutoff for Alzheimer’s disease (AD)
Mini-Mental State Exam was significantly lower in PD compared with normal controls (NC)
Summary
Cognitive impairment (CI) is a common non-motor feature in Parkinson’s disease (PD). 25% of non-demented PD cases have mild CI (MCI), which may precede dementia.[1] Research on the role of central nervous system structural affection and associated molecular mechanisms for cognitive decline in PD is needed for early diagnosis and intervention. Imaging studies in PD have shown different patterns of magnetic resonance imaging (MRI) cortical gray matter atrophy. In PD without dementia, little or no regional thinning has been found in hippocampus, temporal, limbic, frontal, parietal, or occipital cortex, but there are more pronounced changes in PDMCI and widespread atrophy is described in PD with dementia.[2,3,4] Hippocampal atrophy has been associated with CI, especially poorer memory, in PD with and without dementia.[3]
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