Abstract
To investigate the potential applications and the molecular mechanisms of transcranial direct current stimulation (tDCS) on cognitive impairment in a vascular dementia (VD) animal model. Sprague-Dawley rats were used in this study. VD rat model was induced by modified permanent bilateral common carotid artery occlusion (2-VO) approach. Anodal tDCS was applied to the animals. Morris water maze was used to analyze spatial memory and navigation ability. The pathological changes in the hippocampal CA1 region and cerebral cortex were examined via Hematoxylin-Eosin staining. The rats were sacrificed for the measurement of the level of superoxide (SOD), glutathione (GSH), reactive oxidative species (ROS), malondialdehyd (MDA), Interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α level in the hippocampus. Western blot was carried out to measure the hippocampal expression of microtubule-associated protein 1 light chain 3 (LC-3) and p62. Rats with VD have decreased number of neurons in the hippocampus and cerebral cortex, as well as worse cognitive impairment. The proliferation of activated microglia and astroglia, accompanied with attenuation of myelination were observed in the white matter about 1 month after 2-VO operation. These abnormalities were significantly ameliorated by tDCS treatment. Further study revealed that anodal tDCS could suppress the MDA and ROS level, while enhance the SOD and GSH level to reduce the oxidative stress. Anodal tDCS could inhibit hypoperfusion-induced IL-1β, IL-6, and TNF-α expression to attenuate inflammatory response in hippocampus. Moreover, anodal tDCS treatment could alleviate autophagy level. The study has demonstrated a possible therapeutic role of tDCS in the treatment of cognitive impairment in VD.
Highlights
Vascular dementia (VD) is the second most common cause of dementia after Alzheimer’s disease, accounting for around 15% of cases (O’Brien and Thomas, 2015)
Neuroinflammation characterized by Interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)α plays an important role in VD (Belkhelfa et al, 2018)
Sixty standard deviation (SD) rats were randomly divided into three groups: (1) Sham group: Sham operation group treated with sham stimulation, (2) VD group: VD rat models treated with sham stimulation, (3) transcranial direct current stimulation (tDCS) group: VD rat models treated with anodal tDCS
Summary
Vascular dementia (VD) is the second most common cause of dementia after Alzheimer’s disease, accounting for around 15% of cases (O’Brien and Thomas, 2015). Chronic cerebral hypoperfusion played a causative role in VD (Du et al, 2017). Previous studies demonstrated that cerebral hypoperfusion could lead to oxidative stress, neuroinflammation, neurotransmitter system dysfunction, mitochondrial dysfunction, disturbance of lipid metabolism, and alterations of growth factor (Du et al, 2017). Oxidative stress plays an important role in cognitive deficits induced by the chronic cerebral hypoperfusion (Chunjiea et al, 2016). Neuroinflammation characterized by Interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)α plays an important role in VD (Belkhelfa et al, 2018). Decreasing autophagic activity may contribute to cognitive improvement in rats with VD (Liu et al, 2018; Venkat et al, 2018)
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