4.5 Article

Cognitive Sequelae and Hippocampal Dysfunction in Chronic Kidney Disease following 5/6 Nephrectomy

期刊

BRAIN SCIENCES
卷 12, 期 7, 页码 -

出版社

MDPI
DOI: 10.3390/brainsci12070905

关键词

chronic kidney disease; hippocampus; neuronal plasticity; blood-brain barrier; sodium-hydrogen exchangers

资金

  1. Basic Science Research Program [NRF-2018R1D1A1B07043247, NRF-2021R1F1A1060352, NRF-2017R1D1A1B05036195]
  2. National Research Foundation of Korea - Ministry of Education

向作者/读者索取更多资源

Neurological disorders are common in patients with chronic kidney disease (CKD), and vascular factors and uremic toxins are involved in cognitive impairment. However, the pathophysiology of cognitive impairment in CKD patients is not fully understood. This study used rat models to observe the changes in behavior, synaptic plasticity, and immunostaining of the hippocampus during CKD progression. The results suggest that CKD can lead to deficits in cognitive function and alterations in the hippocampus.
Neurological disorders are prevalent in patients with chronic kidney disease (CKD). Vascular factors and uremic toxins are involved with cognitive impairment in CKD. In addition, vascular dementia-induced alterations in the structure and function of the hippocampus can lead to deficits in hippocampal synaptic plasticity and cognitive function. However, regardless of this clinical evidence, the pathophysiology of cognitive impairment in patients with CKD is not fully understood. We used male Sprague Dawley rats and performed 5/6 nephrectomy to observe the changes in behavior, field excitatory postsynaptic potential, and immunostaining of the hippocampus following CKD progression. We measured the hippocampus volume on magnetic resonance imaging scans in the controls (n = 34) and end-stage renal disease (ESRD) hemodialysis patients (n = 42). In four cognition-related behavior assays, including novel object recognition, Y-maze, Barnes maze, and classical contextual fear conditioning, we identified deficits in spatial working memory, learning and memory, and contextual memory, as well as the ability to distinguish familiar and new objects, in the rats with CKD. Immunohistochemical staining of Na+/H+ exchanger1 was increased in the hippocampus of the CKD rat models. We performed double immunofluorescent staining for aquaporin-4 and glial fibrillary acidic protein and then verified the high coexpression in the hippocampus of the CKD rat model. Furthermore, results from recoding of the field excitatory postsynaptic potential (fEPSP) in the hippocampus showed the reduced amplitude and slope of fEPSP in the CKD rats. ESRD patients with cognitive impairment showed a significant decrease in the hippocampus volume compared with ESRD patients without cognitive impairment or the controls. Our findings suggest that uremia resulting from decreased kidney function may cause the destruction of the blood-brain barrier and hippocampus-related cognitive impairment in CKD.

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