Magnesium Increases the Protective Effect of Citicoline on Aluminum Chloride-induced Cognitive Impairment

Abstract

Objective: Alzheimer's disease is a popular neurodegenerative disorder which is growing in the elderly people. Exposure to environmental pollutant like aluminum could trigger or accelerate its involved mechanisms like tau phosphorylation. The current study will evaluate the effect of alone or co-administration of Citicoline or/and magnesium on the aluminum chloride induced memory impairment. Methods: Male albino mice were randomly divided into different groups (n = 7). Memory impairment was induced via orally administration of 300 mg/kg Aluminum Chloride for 28 days. Based on respective group, animals received 100, 250, 500 mg/kg of Citicoline or 50, 100, 150 mg/kg of Magnesium sulfate (MgSO4), intraperitoneally. In co-administration, 50 mg/kg of MgSO4 injected concomitantly with 100, 250, or 500 mg/kg of Citicoline. Rivastigmine (2 mg/kg intraperitoneally) was used as a positive control. Memory was evaluated using the Object Recognition Task (ORT) and Passive Avoidance Test (PAT). Results: The studied doses of Citicoline or MgSO4 when administered individually showed significant increase in the discrimination index in ORT and latency time in the PAT compared to the Aluminium chloride (AlCl3) treated group. Concomitant injection of 50 mg/kg MgSO4 with the different doses of Citicoline strongly increased the above indices values in comparison to each alone. Conclusion: The findings show, individual administration of Citicoline or MgSO4 inverted the AlCl3-induced memory impairment in a dose independent manner. The addition of MgSO4 to the Citicoline showed a synergistic effect in the PAT and likely additive effect in the ORT.

Brain Targeting of Citicoline Sodium via Hyaluronic Acid-Decorated Novel Nano-Transbilosomes for Mitigation of Alzheimer’s Disease in a Rat Model: Formulation, Optimization, in vitro and in vivo Assessment

“…Previous data represent that AlCl 3 -induced memory impairment is thought to be caused by a variety of ways 124 AlCl 3 cognitive toxicities have been linked to the upregulation of APP, Ab, NF-kB, AChE activity, nitric oxide release, oxidative stress, and the eventual neuronal apoptosis. 125 , 126 …”

The Effect of Remifentanil, MgSO4, or Remifentanil-MgSO4 as Neuroprotectors on BDNF, MAC, and Caspase-3 Levels in Wistar Rats with Traumatic Brain Injury

“…This treatment reduced the apoptotic process by maintaining retinal ganglion cell and reducing the expression of vascular endothelial growth factor receptor-2 as well as glial fibrillary acidic protein (GFAP) [10], [28]. Another study showed that MgSO 4 has a protective effect on brain tissues of preeclampsia rat models by inhibiting signaling pathway of nuclear factor-κB (NF-κB)/intercellular adhesion molecule-1 [29] In rat models with cognitive disorders induced by aluminum chloride, the administration of MgSO 4 improved memory dysfunction [30]. Another study found that remifentanil or MgSO 4 when combined with sevoflurane produced adequate hypotensive anesthetic level.…”

Real-world Evaluation of Tolerability, Safety and Efficacy of Rivastigmine Oral Solution in Patients with Mild to Moderate Alzheimer's Disease Dementia

“…Nearly 90% of AD patients presented with BPSD, leading to independence reduction and incapability of completing daily activities. These might have impacts on medication adherence, tolerability and efficacy [ 35 ]. The overall adherence was 80.6% in our study.…”

“…In consideration of treating AD, BPSD is an important issue. BPSD lead to poor outcomes, distress among patients and caregivers, earlier placement in nursing homes, long-term hospitalization, misuse of medication, and increased health care costs [ 35 , 50 ]. Whether the oral solution benefits more than the conventional oral capsule in management of BPSD requires further evalua-tion.…”