Ceftriaxone prevents the neurodegeneration and decreased neurogenesis seen in a Parkinson’s disease rat model: An immunohistochemical and MRI study

Weng, Jun‐Cheng; Tikhonova, Maria A.; Chen, Jian-Horng; Shen, Mei-Shiuan; Meng, Wan-Yun; Chang, Yen-Ting; Chen, Ke-Hsin; Liang, Keng Chen; Hung, Chi‐Feng; Amstislavskaya, Tamara G.; Ho, Ying-Jui

doi:10.1016/j.bbr.2016.02.034

Cited by 35 publications

(38 citation statements)

References 86 publications

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“…As such, MEMRI signal is directly related to neural viability and activity [44,45]. To date, some studies have utilized MEMRI for studying pathobiology of neurodegenerative diseases, such as PD [46][47][48][49]. However, neurodegeneration is a dynamic process rather than a static event.…”

Section: Discussionmentioning

confidence: 99%

Manganese-Enhanced Magnetic Resonance Imaging for Detection of Vasoactive Intestinal Peptide Receptor 2 Agonist Therapy in a Model of Parkinson's Disease

et al. 2016

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Neuroprotective immunity is defined by transformation of T-cell polarity for therapeutic gain. For neurodegenerative disorders and specifically for Parkinson's disease (PD), granulocyte-macrophage colony stimulating factor or vasoactive intestinal peptide receptor 2 (VIPR2) agonists elicit robust anti-inflammatory microglial responses leading to neuronal sparing in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxicated mice. While neurotherapeutic potential was demonstrated for PD, there remain inherent limitations in translating these inventions from the laboratory to patients. One obstacle in translating such novel neurotherapeutics centers on the availability of suitable noninvasive methods to track disease progression and therapeutic efficacy. To this end, we developed manganese-enhanced magnetic resonance imaging (MEMRI) assays as a way to track a linkage between glial activation and VIPR2 agonist (LBT-3627)-induced neuroprotective immunity for MPTP-induced nigrostriatal degeneration. Notably, LBT-3627-treated, MPTP-intoxicated mice show reduced MEMRI brain signal intensities. These changes paralleled reduced astrogliosis and resulted in sparing of nigral tyrosine hydroxylase neurons. Most importantly, the data suggest that MEMRI can be developed as a biomarker tool to monitor neurotherapeutic responses that are relevant to common neurodegenerative disorders used to improve disease outcomes.

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Section: Discussionmentioning

confidence: 99%

Manganese-Enhanced Magnetic Resonance Imaging for Detection of Vasoactive Intestinal Peptide Receptor 2 Agonist Therapy in a Model of Parkinson's Disease

et al. 2016

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“…Weng et al [114] reported that ceftriaxone prevented the loss of neuronal activity and decreased the neurogenesis in the brain of PD rats. Sharma et al [115] suggested that administration of quercetin attenuated the neuronal death and reduced the oxidative stress in aluminium-induced neurodegeneration in the rat hippocampus.…”

Section: Natural Products and Parkinson's Diseasementioning

confidence: 99%

The Role of Reactive Oxygen Species in the Pathogenesis of Alzheimer’s Disease, Parkinson’s Disease, and Huntington’s Disease: A Mini Review

Manoharan

Guillemin

Abiramasundari

et al. 2016

Oxidative Medicine and Cellular Longevity

374

268

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Neurodegenerative diseases affect not only the life quality of aging populations, but also their life spans. All forms of neurodegenerative diseases have a massive impact on the elderly. The major threat of these brain diseases includes progressive loss of memory, Alzheimer's disease (AD), impairments in the movement, Parkinson's disease (PD), and the inability to walk, talk, and think, Huntington's disease (HD). Oxidative stress and mitochondrial dysfunction are highlighted as a central feature of brain degenerative diseases. Oxidative stress, a condition that occurs due to imbalance in oxidant and antioxidant status, has been known to play a vital role in the pathophysiology of neurodegenerative diseases including AD, PD, and HD. A large number of studies have utilized oxidative stress biomarkers to investigate the severity of these neurodegenerative diseases and medications are available, but these only treat the symptoms. In traditional medicine, a large number of medicinal plants have been used to treat the symptoms of these neurodegenerative diseases. Extensive studies scientifically validated the beneficial effect of natural products against neurodegenerative diseases using suitable animal models. This short review focuses the role of oxidative stress in the pathogenesis of AD, PD, and HD and the protective efficacy of natural products against these diseases.

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“…Besides, unlike saline received group, CEF treated group showed an intact density of DAergic neurons in the SNc and DAergic terminals in the striatum. Weng et al, 2016 In vitro study: astrocytes exposed to a neurotoxin, 1-methyl-4-phenyl-pyridinium The cytoprotective actions of CEF is mediated through downregulation of NF-κB and JNK/c-Jun Signaling.…”

Section: Malementioning

confidence: 99%

Repurposing of the β-Lactam Antibiotic, Ceftriaxone for Neurological Disorders: A Review

2019

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To date, there is no cure or disease-modifying agents available for most well-known neurological disorders. Current therapy is typically focused on relieving symptoms and supportive care in improving the quality of life of affected patients. Furthermore, the traditional de novo drug discovery technique is more challenging, particularly for neurological disorders. Therefore, the repurposing of existing drugs for these conditions is believed to be an efficient and dynamic approach that can substantially reduce the investments spent on drug development. Currently, there is emerging evidence that suggests the potential effect of a beta-lactam antibiotic, ceftriaxone (CEF), to alleviate the symptoms of different experimentally-induced neurological disorders: Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, epileptic-seizure, brain ischemia, traumatic brain injuries, and neuropathic pain. CEF also affects the markers of oxidative status and neuroinflammation, glutamatergic systems as well as various aggregated toxic proteins involved in the pathogenesis of different neurological disorders. Moreover, it was found that CEF administration to drug dependent animal models improved the withdrawal symptoms upon drug discontinuation. Thus, this review aimed to describe the effects of CEF against multiple models of neurological illnesses, drug dependency, and withdrawal. It also emphasizes the possible mechanisms of neuroprotective actions of CEF with respective neurological maladies.

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Ceftriaxone prevents the neurodegeneration and decreased neurogenesis seen in a Parkinson’s disease rat model: An immunohistochemical and MRI study

Cited by 35 publications

References 86 publications

Manganese-Enhanced Magnetic Resonance Imaging for Detection of Vasoactive Intestinal Peptide Receptor 2 Agonist Therapy in a Model of Parkinson's Disease

Manganese-Enhanced Magnetic Resonance Imaging for Detection of Vasoactive Intestinal Peptide Receptor 2 Agonist Therapy in a Model of Parkinson's Disease

The Role of Reactive Oxygen Species in the Pathogenesis of Alzheimer’s Disease, Parkinson’s Disease, and Huntington’s Disease: A Mini Review

Repurposing of the β-Lactam Antibiotic, Ceftriaxone for Neurological Disorders: A Review

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