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A Machine Learning Approach to Design an Efficient Selective Screening of Mild Cognitive Impairment
Published on: January 11, 2020
Effects of MFHAS1 on cognitive impairment and dendritic pathology in the hippocampus of septic rats
Jing Zhong1, Chenyue Guo1, Wenting Hou1
1Department of Anesthesiology, Fudan University Shanghai Cancer Center, Shanghai, China; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Aims:
To investigate the effects of malignant fibrous histiocytoma amplified sequence 1 (MFHAS1) on cognitive dysfunction, the expression of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and amyloid β peptide (Aβ) in the hippocampus, as well as dendritic pathology in the hippocampal CA1 region in sepsis-associated encephalopathy (SAE) rats.
Main Methods:
The rats were randomly divided into four groups: 1) control group (subjected to sham surgery), 2) control plus Mfhas1 siRNA group (rats received intracerebroventricular injection of Mfhas1 siRNA after sham surgery), 3) CLP plus control siRNA group (rats received intracerebroventricular injection of control siRNA after cecal ligation and puncture (CLP)), 4) CLP plus Mfhas1 siRNA group (rats received intracerebroventricular injection of Mfhas1 siRNA after CLP). The learning and memory capabilities of the rats were examined by means of fear conditioning and Barnes maze test. The concentration of TNF-α and IL-1β was determined by enzyme-linked immunosorbent assay. The efficiency of siRNA transfection, MFHAS1 and Aβ expression were detected by Western blotting. Total branch lengths of pyramidal dendrites of the CA1 basilar trees and spine density were determined by Golgi staining.
Key Findings:
We observed that MFHAS1 knock-down by Mfhas1 siRNA intracerebroventricular injection could improve cognitive impairment, reduce the expression of TNF-α, IL-1β and Aβ in the hippocampus induced by CLP, and alleviate the dendritic spinal loss of the pyramidal neurons, as well as increase the dendritic branching of the CA1 basilar trees of septic rats.
Significance:
MFHAS1 knock-down can alleviate cognitive impairment, neuroinflammation and dendritic spinal loss in SAE rats.
Insights
Knocking down malignant fibrous histiocytoma amplified sequence 1 (MFHAS1) in sepsis-associated encephalopathy (SAE) rats improved cognitive function. This intervention reduced neuroinflammation and dendritic pathology in the hippocampus.
Area of Science:
- Neuroscience
- Molecular Biology
- Pathology
Background:
- Sepsis-associated encephalopathy (SAE) is a complex neurological disorder characterized by cognitive dysfunction.
- The role of specific molecular pathways, such as malignant fibrous histiocytoma amplified sequence 1 (MFHAS1), in SAE pathogenesis is not fully understood.
- Investigating molecular targets is crucial for developing therapeutic strategies against SAE-induced cognitive deficits.
Purpose of the Study:
- To determine the impact of MFHAS1 on cognitive impairment in SAE rats.
- To assess the effects of MFHAS1 modulation on neuroinflammatory markers (TNF-α, IL-1β) and amyloid-beta (Aβ) deposition in the hippocampus.
- To examine the influence of MFHAS1 on dendritic pathology within the hippocampal CA1 region.
Main Methods:
- Rats were subjected to cecal ligation and puncture (CLP) to induce sepsis or sham surgery.
- Intracerebroventricular injection of MFHAS1 siRNA or control siRNA was administered.
- Cognitive function was evaluated using fear conditioning and Barnes maze tests.
- Hippocampal levels of TNF-α, IL-1β, and Aβ were quantified using ELISA and Western blotting.
- Dendritic morphology and spine density were analyzed via Golgi staining.
Main Results:
- MFHAS1 knockdown significantly improved learning and memory deficits in SAE rats.
- Reduced expression of pro-inflammatory cytokines TNF-α and IL-1β was observed in the hippocampus following MFHAS1 knockdown.
- Amyloid-beta (Aβ) peptide levels were decreased in the hippocampus of rats with MFHAS1 knockdown.
- Alleviation of dendritic spine loss and increased dendritic branching in the hippocampal CA1 region were noted.
Conclusions:
- MFHAS1 plays a significant role in the development of cognitive impairment and neuroinflammation in SAE.
- Targeting MFHAS1 through siRNA-mediated knockdown offers a potential therapeutic approach to mitigate SAE-induced neurological damage.
- Further research into MFHAS1's molecular mechanisms could lead to novel treatments for sepsis-related brain dysfunction.
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