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Osteoporotic thoracolumbar fractures
Published in Peter V. Giannoudis, Thomas A. Einhorn, Surgical and Medical Treatment of Osteoporosis, 2020
Bisphosphonates are the most prescribed drugs to treat osteoporosis (25). They are also widely used to treat pain arising from metastatic cancer involving the skeletal sites and bone pain from Paget disease. Similar to calcitonin, the exact analgesic mechanism of bisphosphonate is unclear. Bisphosphonates work by inhibiting osteoclast activity and resorption of bone (26). It also has anti-interleukin (IL)-1, IL-6, and anti-tumor necrosis factor alpha (anti-TNF-α) properties that dampen the inflammatory process (26,27). Hence, it is hypothesized that the reduction in osteoclast activity, i.e., the rate of osteolysis, and local anti-inflammatory effect result in pain relief (27). Besides that, the analgesic response seen in animal models after intracerebroventricular injection of clodronate also points toward a central nociceptive effect (27). Not all bisphosphonates have demonstrated the same degree of pain relief, as trials in animal studies reported varying degrees of pain-relieving response with different bisphosphonates (27,28).
Postulated Physiological and Pathophysiological Roles on Motility
Published in Edwin E. Daniel, Neuropeptide Function in the Gastrointestinal Tract, 2019
Hans-Dieter Allescher, Sultan Ahmad
When the MMC activity in the upper gut was interrupted by i.v. infusion of gastrin or CCK and a digestive motility pattern of irregular activity was produced, the cycling changes of motilin were not abolished.641 A similar result was obtained when the MMC was interrupted by intracerebroventricular injection of CRF.664 This indicates that cyclic changes of motilin are not sufficient to induce MMC activity and that the cyclic changes of motilin are unlikely to be only the consequence of the cyclic motility changes during the MMC, as postulated.665,660
Experimental Models of Status Epilepticus
Published in Steven L. Peterson, Timothy E. Albertson, Neuropharmacology Methods in Epilepsy Research, 2019
Intracerebral or intraventricular injection of kainic acid results in a more restricted and a more easily duplicated pattern of neuronal damage than when kainic acid is administered systemically. Intracerebroventricular injection consistently results in hippocampal damage localized to CA3 pyramidal neurons.10
Pharmacokinetic improvement provided by microneedle patch in delivering bee venom, a case study in combating scopolamine-induced neurodegeneration in mouse model
Published in Drug Delivery, 2022
Cong Duc Nguyen, Jaehee Yoo, Eun Jin An, Chang Yub Sung, Do Hyeon Jeong, Soo-Yeon Park, Jae-Hong Kim, Gihyun Lee
About the in vivo model used in the research: The scopolamine-induced neuro stress model is a common model for studying neurodegenerative disorders in mice. The result of scopolamine stress includes a rise in ROS and MDA levels, decrease in the levels of APT in the brain, and influent overall cognitive and locomotor function which can be scored via open field maze, and long term memory ability which can be evaluated by water maze (J. S. Lee et al., 2015; Karthivashan et al., 2018; Baghel & Thakur, 2019; Model et al., 2019; Muhammad et al., 2019; Baek et al., 2020; Al-Amin et al., 2022). For the current study, we analyzed the melittin as a marker chemical compound present in the brain tissue of the mice. We believe that scopolamine-induced mice (achieved via the intraperitoneal route at the abdominal area) avoids possible brain damages, better than to utilize models with methods that create an Alzheimer-like state by administrating amyloid beta or lipopolysaccharides delivered by intracerebroventricular injections directly into the brains. Such an invasive intracerebroventricular injection might affect the brain blood barrier—which controls the passing of large molecule such as melittin—and influences the overall reliability of the analysis.
Stereotaxic-assisted gene therapy in Alzheimer’s and Parkinson’s diseases: therapeutic potentials and clinical frontiers
Published in Expert Review of Neurotherapeutics, 2022
Samar O. El Ganainy, Tony Cijsouw, Mennatallah A. Ali, Susanne Schoch, Amira Sayed Hanafy
Despite the ongoing research, the clinical trials investigating the therapeutic potentials of gene-editing modalities utilizing stereotaxis are still lagging. In Figure 2, we highlight the frequently targeted genes to manage AD and PD using different gene-editing platforms, demonstrating the huge gap between preclinical and clinical studies implementing stereotaxic interventions as well as studies that involved systemic administration solely. In the meantime, the intracerebroventricular injection is applied in preclinical studies for alleviating the symptoms of PD and AD [166,183]. However, convection-enhanced delivery, which is a technique used for direct intracranial application of different agents, requires the use of an appropriate catheter and infusion flow-rate. The lack of validated catheter systems and the risk of errors and complications hinder the bridging of the gap between animal and human studies [184]. Furthermore, it would be highly beneficial if the stereotaxic therapy could be limited to a single procedure.
Alzheimer’s disease: microglia targets and their modulation to promote amyloid phagocytosis and mitigate neuroinflammation
Published in Expert Opinion on Therapeutic Targets, 2020
Microglia implications in CNS abnormalities such as AD has become a promising therapeutic avenue. The research has produced a notable body of literature describing a broad repertoire of potential pharmacological inducers and suppressors [142]. Most of these approaches protect against the harmful effects of neuroinflammation, whether by upregulating repressors of microglial activation or by blocking microglia‐mediated pro-inflammatory signals or substances. Fewer studies focus on upregulating microglial repair and remodeling [143]. Significant limitations, both biologically and technically to study microglia which impede the progress of research in this avenue. For instance, the BBB [144] acts as a giant obstacle; the permeability of the BBB is selective for only certain substances such as nutrients and water [145]. Thus, the barrier prevents the passage of certain drugs and therapeutic agents required for the treatment of AD and the other neurodegenerative diseases [146]. One possible intervention to overcome BBB in AD experimental animal models is to deliver the tested drug directly to the brain via intracerebroventricular injection (ICV). Unfortunately, the chronic nature of AD needs a prolonged protocol of injections. ICV is too problematic for such chronic protocol.