https://scholars.lib.ntu.edu.tw/handle/123456789/520115
標題: | A new avenue for treating neuronal diseases: Ceftriaxone, an old antibiotic demonstrating behavioral neuronal effects | 作者: | CHUN-HWEI TAI Bellesi M. Chen A.-C. Lin C.-L. Li H.-H. Lin P.-J. Liao W.-C. Hung C.-S. Schwarting R.K. Ho Y.-J. |
關鍵字: | Alzheimer's disease; Ceftriaxone; Dementia with Lewy bodies; Neurodegenerative disorders; Parkinson's disease dementia | 公開日期: | 2019 | 出版社: | Elsevier B.V. | 卷: | 364 | 起(迄)頁: | 149-156 | 來源出版物: | Behavioural Brain Research | 摘要: | Several neurodegenerative disorders, namely Parkinson's disease dementia, dementia with Lewy bodies, and Alzheimer's disease, share common pathophysiological features, such as (1) cognitive deficits, (2) glutamatergic hyperactivity-related excitotoxicity, and (3) deposition of α-synuclein (α-syn) and β-amyloid (Aβ). Ceftriaxone (CEF) is a well-tested and safe drug that has been used as an antibiotic for several decades. Recent studies have demonstrated the following effects of CEF: (1) increasing glutamate transporter-1 expression and glutamate reuptake and suppressing excitotoxicity, (2) binding well with α-syn and inhibition of α-syn polymerization, (3) modulating expression of genes related to Aβ metabolism, and (4) enhancing neurogenesis and recovery of neuronal density. In addition, our data revealed that CEF ameliorates seizure and abnormal neuronal firing in the brain. These results suggest the potential of CEF in treating neuronal disorders. This paper addresses the effects and pharmacology of CEF. ? 2019 Elsevier B.V. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85061637366&doi=10.1016%2fj.bbr.2019.02.020&partnerID=40&md5=e21431ead9ed5d519a49b9a327cdc5ca https://scholars.lib.ntu.edu.tw/handle/123456789/520115 |
ISSN: | 0166-4328 | DOI: | 10.1016/j.bbr.2019.02.020 | SDG/關鍵字: | alpha synuclein; amyloid beta protein; ceftriaxone; ceftriaxone; neuroprotective agent; Alexander disease; apoptosis; brain ischemia; cell survival; degenerative disease; dementia; diffuse Lewy body disease; drug effect; drug mechanism; excitotoxicity; human; nerve cell; nervous system development; neurotransmission; nonhuman; oxidative stress; pain; Parkinson disease; polymerization; priority journal; protein protein interaction; rat model; Review; seizure; theta rhythm; treatment planning; Alzheimer disease; brain; degenerative disease; diffuse Lewy body disease; metabolism; neurologic disease; Parkinson disease; Alzheimer Disease; Brain; Ceftriaxone; Humans; Lewy Body Disease; Nervous System Diseases; Neurodegenerative Diseases; Neurogenesis; Neurons; Neuroprotective Agents; Parkinson Disease |
顯示於: | 醫學系 |
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