Ceftriaxone Treatment for Neuronal Deficits: A Histological and MEMRI Study in a Rat Model of Dementia with Lewy Bodies

Author:

Ho Ying-Jui1ORCID,Weng Jun-Cheng23,Lin Chih-Li4ORCID,Shen Mei-Shiuan1,Li Hsin-Hua4,Liao Wen-Chieh56,Tsai Nu-Man7,Hung Ching-Sui8ORCID,Lai Te-Jen49ORCID,Lee I-Yen10ORCID

Affiliation:

1. Department of Psychology, Chung Shan Medical University Hospital, Chung Shan Medical University, Taichung 402, Taiwan

2. Department of Medical Imaging and Radiological Sciences, Chang Gung University, Taoyuan 33302, Taiwan

3. Department of Psychiatry, Chang Gung Memorial Hospital, Chiayi 613, Taiwan

4. Institute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan

5. Department of Anatomy, Faculty of Medicine, Chung Shan Medical University, Chung Shan Medical University Hospital, Taichung 402, Taiwan

6. Department of Pediatrics, Chung Shan Medical University Hospital, Taichung 402, Taiwan

7. School of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung 402, Taiwan

8. Occupational Safety and Health Office, Taipei City Hospital, Taipei 10341, Taiwan

9. Department of Psychiatry, Chung Shan Medical University Hospital, Chung Shan Medical University, Taichung 402, Taiwan

10. Division of Urology, Department of Surgery, Tungs’ Taichung Metroharbor Hospital, Taichung 43503, Taiwan

Abstract

Dementia with Lewy bodies (DLB) is characterized by neuronal deficits and α-synuclein inclusions in the brain. Ceftriaxone (CEF), a β-lactam antibiotic, has been suggested as a therapeutic agent in several neurodegenerative disorders for its abilities to counteract glutamate-mediated toxicity and to block α-synuclein polymerization. By using manganese-enhanced magnetic resonance imaging (MEMRI) and immunohistochemistry, we measured the effects of CEF on neuronal activity and α-synuclein accumulation in the brain in a DLB rat model. The data showed that CEF corrected neuronal density and activity in the hippocampal CA1 area, suppressed hyperactivity in the subthalamic nucleus, and reduced α-synuclein accumulation, indicating that CEF is a potential agent in the treatment of DLB.

Funder

Ministry of Science and Technology

Publisher

Hindawi Limited

Subject

Neurology (clinical),Neurology,General Medicine,Neuropsychology and Physiological Psychology

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