Repurposing of the β-Lactam Antibiotic, Ceftriaxone for Neurological Disorders: A Review
Open accessAbstract
So far there is no cure or disease-modifying agents available for most of the well-known neurological disorders and therapy is typically focused on relieving symptoms and supportive care to improve the quality of life of the patients. Besides, the traditional de novo drug discovery technique, particularly for neurological disorders, is more challenging hence repurposing of existing drugs for these conditions are supposed to be an efficient and dynamic approach that can substantially reduce the investment spent during drug development. Currently, there is emerging evidence that suggests the potential of a beta-lactam antibiotic, ceftriaxone to alleviate the symptoms of different experimentally-induced neurological disorders, such as Parkinson’s disease, Alzheimer’s disease, amyotrophic lateral sclerosis, epileptic-seizure, brain ischemia, traumatic brain injuries, and neuropathic pain. Ceftriaxone also affects the markers of oxidative status and neuro-inflammation, glutamatergic systems as well as various aggregated toxic proteins involved in the pathogenesis of different neurological disorders. Moreover, ceftriaxone administration to animal models of drug dependency was found to improve the withdrawal symptoms upon drug discontinuation. Thus, this review aimed to describe the effects of ceftriaxone against multiple models of neurological illnesses, drug dependency, and withdrawal. It also emphasizes the possible mechanisms of neuroprotective actions of ceftriaxone with respective neurological maladies.
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Ceftriaxone exhibits a neuroprotective effect in AD.
“it exhibits a neuroprotective effect in addition to its antibacterial effect in PD [15, 20] and AD [21].”
From Neuroprotective Effect of Ceftriaxone on MPTP‐Induced Parkinson’s Disease Mouse Model by Regulating Inflammation and Intestinal Microbiota (2021) · cites this paper as [21]
Ceftriaxone (CTX) is a β-lactam antibiotic with a strong and safe past record.
“Ceftriaxone (CTX) is a β-lactam antibiotic with a strong and safe past record [225,226].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [225]
Treatment of several PD animal models with CTX stimulates neurogenesis.
“The treatment of several PD animal models with CTX is known to improve neuroinflammatory and oxidative stress markers, stimulate neurogenesis and promote astrocyte viability through the suppression of NF-κB/c-Jun-mediated signaling [225,226,227,228].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [225]
Treatment of several PD animal models with CTX promotes astrocyte viability.
“The treatment of several PD animal models with CTX is known to improve neuroinflammatory and oxidative stress markers, stimulate neurogenesis and promote astrocyte viability through the suppression of NF-κB/c-Jun-mediated signaling [225,226,227,228].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [225]
Treatment of several PD animal models with CTX improves neuroinflammatory markers.
“The treatment of several PD animal models with CTX is known to improve neuroinflammatory and oxidative stress markers, stimulate neurogenesis and promote astrocyte viability through the suppression of NF-κB/c-Jun-mediated signaling [225,226,227,228].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [225]
Treatment of several PD animal models with CTX improves oxidative stress markers.
“The treatment of several PD animal models with CTX is known to improve neuroinflammatory and oxidative stress markers, stimulate neurogenesis and promote astrocyte viability through the suppression of NF-κB/c-Jun-mediated signaling [225,226,227,228].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [225]
CTX suppresses NF-κB/c-Jun-mediated signaling.
“The treatment of several PD animal models with CTX is known to improve neuroinflammatory and oxidative stress markers, stimulate neurogenesis and promote astrocyte viability through the suppression of NF-κB/c-Jun-mediated signaling [225,226,227,228].”
From The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment (2022) · cites this paper as [225]
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- Authors
- Yimer, E. M., Hishe, H. Z., & Tuem, K. B.
- Affiliations
- Mekelle University (ET)
- Corresponding author
- Yimer, Ebrahim M.
- Venue
- Frontiers in Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2019-03-26
- Volume
- 13
- Pages
- 236-236
- ISSN
- 1662-453X (ISSN-L)
- PMC
- PMC6444273
- OpenAlex
- W2923249856
- Cited by
- 72
- References
- 136
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 5 · 2023: 9 · 2022: 8 · 2021: 17 · 2020: 15 · 2019: 2
- FWCI
- 1.09
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- ceftriaxone, drug repurposing, neurological disorders, neuroprotection, Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, epileptic seizures, cerebral ischemia, traumatic brain injury, neuropathic pain, oxidative stress, neuroinflammation, glutamatergic system, protein aggregation, drug addiction, withdrawal symptoms
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