Longitudinal volume changes of hippocampal subfields and cognitive decline in Parkinson’s disease

Rui Xu, Xiaofei Hu, Xiaomei Jiang, Yanling Zhang, Jian Wang, Xianchun Zeng


Background: Neuropathological studies have shown that the hippocampus is affected in Parkinson’s disease (PD) with cognitive impairment. Our goal was to assess the longitudinal volume change of different hippocampal subfields in PD patients with and without cognitive decline using magnetic resonance imaging (MRI).
Methods: A total of 28 nondemented PD patients and 27 neurologically unimpaired elderly controls were enrolled in this study, and three-dimensional (3D) T1-weighted MRI was performed. All PD patients that were followed up and rescanned after 2 years were divided into two groups: PD without cognitive decline (n=15) and PD with cognitive decline (n=13). A Bayesian model implemented in FreeSurfer was used to segment the hippocampal subfields automatically. Scale for global cognitive status included the Mini Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA).
Results: In the cross sectional study, the bilateral hippocampal volume was smaller in PD patients compared to healthy controls, and the bilateral subiculum, CA2/3, CA4, and molecular layer (ML) subfields, and the right granule cell layer of the dentate gyrus (GC-DG) subfield, were significantly decreased in the PD patients. Significant correlations were found between the MoCA score and total hippocampus volume in PD patients. In the follow-up group, bilateral CA4, ML, and GC-DG subfields, and left CA2/3 and right presubiculum subfields, were significantly smaller in PD patients with cognitive decline compared to PD patients without cognitive decline. Significant correlations were found between the longitudinal change of the MMSE or MoCA scores and percent change rate of total bilateral hippocampal, bilateral ML, and right CA4 in all PD patients.
Conclusions: Our results demonstrated the selective regional vulnerability of the hippocampus in the progression of PD. These findings corroborate neuropathological findings and add novel information about the involvement of the hippocampus in the cognitive dysfunction of PD.