Memantine prevents aluminum-induced cognitive deficit in rats

Abdel-Aal, Raafat A.; Assi, Abdel-Azim; Kostandy, Botros B.

doi:10.1016/j.bbr.2011.06.031

Cited by 18 publications

(6 citation statements)

References 60 publications

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“…The cognitive impairment model induced by aluminum resulted in the worst performance in the MWM and lowest DI in the NOR test, reflecting spatial, working, and short-term memory problems consistent with Al-induced neurobehavioral changes reported in the literature. − …”

Section: Discussionsupporting

confidence: 74%

Docosahexaenoic Acid (DHA), Vitamin D3, and Probiotics Supplementation Improve Memory, Glial Reactivity, and Oxidative Stress Biomarkers in an Aluminum-Induced Cognitive Impairment Rat Model

Faccinetto-Beltrán,

Reza-Zaldivar,

Curiel-Pedraza

et al. 2024

ACS Omega

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Globally, the rise in neurodegenerative issues in tandem with shifts in lifestyle and aging population has prompted a search for effective interventions. Nutraceutical compounds have emerged as promising agents for addressing these challenges. This 60-day study on an aluminum-induced cognitive impairment rat model assessed three compounds and their combinations: probiotics (Prob, Lactobacillus plantarum [5 × 10 10 CFU/day], and Lactobacillus acidophilus [5 × 10 10 CFU/day]), docosahexaenoic acid (DHA, 23.8 mg/day), and vitamin D3 (VD3, 150 IU/day). Behavioral outcomes were evaluated by using the Morris water maze and novel object recognition tests. Glial activation was assessed through immunofluorescence analysis of GFAP/Iba1, and oxidative stress markers in brain tissue were determined by measuring the levels of Malondialdehyde (MDA) and Superoxide dismutase (SOD). The results demonstrated a progressive improvement in the learning and memory capacity. The aluminum group exhibited the poorest performance in the behavioral test, enhanced GFAP/Iba1 activation, and elevated levels of oxidative stress markers. Conversely, the DHA + Prob + VD3 treatment demonstrated the best performance in the Morris water maze. The combination of DHA + Prob + VD3 exhibited superior performance in the Morris water maze, accompanied by reduced levels of GFAP/Iba1 activation in DG/CA1 brain regions. Furthermore, DHA + Prob supplementation showed lower GFAP/Iba1 activation in the CA3 region and enhanced antioxidant activity. In summary, supplementing various nutraceutical combinations, including DHA, VD3, and Prob, displayed notable benefits against aluminum-induced cognitive impairment. These benefits encompassed memory enhancement, diminished MDA concentration, increased SOD activity, and reduced glial activation, as indicated by GFAP/ Iba1 markers.

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Section: Discussionsupporting

confidence: 74%

Docosahexaenoic Acid (DHA), Vitamin D3, and Probiotics Supplementation Improve Memory, Glial Reactivity, and Oxidative Stress Biomarkers in an Aluminum-Induced Cognitive Impairment Rat Model

Faccinetto-Beltrán,

Reza-Zaldivar,

Curiel-Pedraza

et al. 2024

ACS Omega

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“…The use of memantine in mice infected with JEV can prolong the survival of mice. In another study, memantine was effective at protecting neurons when used at a dose of 20 mg/kg . However, when memantine was used excessively, it may adversely affect the health of mice .…”

Section: Discussionmentioning

confidence: 99%

Memantine can relieve the neuronal impairment caused by neurotropic virus infection

Sun

Zhou

Liu

et al. 2019

Journal of Medical Virology

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Neurotropic viruses, such as the rabies virus (RABV) and Japanese encephalitis virus (JEV), induce neuronal dysfunction and complication, causing neuronal damage. Currently, there are still no effective clinical treatments for neuronal injury caused by neurotropic viruses. Memantine, a drug capable of passing through the blood‐brain barrier, noncompetitively and reversibly binds to n‐methyl‐ d‐aspartic acid (NMDA) receptors. Memantine is used to treat Alzheimer's disease by blocking the activation of extra axonal ion channels, thus preventing neuronal degeneration by inhibiting the abnormal cytosolic Ca 2+ increase. To explore whether memantine can alleviate neurological disturbances caused by RABV and JEV, the following experiments were carried out: (1) for primary neurons cultured in vitro infected with RABV, the addition of memantine showed neuroprotection. (2) In the RABV challenge experiments, memantine had limited therapeutic effect, mildly extending the survival time of mice. In contrast, memantine significantly prolonged the survival time of mice infected with JEV, by reducing the intravascular cuff and inflammatory cell infiltration in mice. Furthermore, memantine decreases the amount of JEV virus in mice brain.

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“…The designs of exploratory studies (e.g., Abdel-Aal et al 2011a, 2011b, Abu-Taweel et al 2011a, 2011b, Akiyama et al 2012, Cheng et al 2012, Cui et al 2012, Elsaid et al 2011, Garrosa et al 2011, Kumar et al 2011, Moselhy et al 2011, Sun et al 2011b, Thirunavukkarasu et al 2010, 2011, 2012, Viezeliene et al 2011, 2012, Wang et al 2010a, Xiao et al 2011) and of even those that meet current regulatory guidelines (e.g., Hirata-Koizumi et al 2011a, 2011b) failed to include concurrent controls treated in an identical manner with equimolar doses of the hydrolysis products (e.g., HCl, H 2 SO 4 ). It is clear these hydrolysis products confound the interpretation of in vivo (e.g., Hirata-Koizumi et al 2011a) and in vitro (Castorina et al 2010, Cifone et al 1987, Güngör et al 2010, Kamalov et al 2011, Morita et al 1989, 1992) data, particularly where media Al concentrations ≥ 10 μM are equivalent to lethal or near-lethal serum Al concentrations in humans (Krewski et al 2007).…”

Section: Synthesis and Conclusionmentioning

confidence: 99%

Systematic review of potential health risks posed by pharmaceutical, occupational and consumer exposures to metallic and nanoscale aluminum, aluminum oxides, aluminum hydroxide and its soluble salts

Willhite¹,

Karyakina²,

Yokel³

et al. 2014

Critical Reviews in Toxicology

316

201

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Aluminum (Al) is a ubiquitous substance encountered both naturally (as the third most abundant element) and intentionally (used in water, foods, pharmaceuticals, and vaccines); it is also present in ambient and occupational airborne particulates. Existing data underscore the importance of Al physical and chemical forms in relation to its uptake, accumulation, and systemic bioavailability.Address for correspondence: Calvin C. Willhite, Risk Sciences International, 55 Metcalfe Street, Suite 700, Ottawa, ON, Canada. calvinwillhite@hotmail.com. Declaration of interestPartial funding for this work was provided by a contract to review the recent scientific literature on health effects of aluminum between the International Aluminium Institute (IAI, www.world-aluminium.org), the Aluminium Reach Consortium (ARC, www.aluminium-reach-consortium.eu), and Risk Sciences International (RSI, www.risksciences.com), a Canadian company established in 2006 in partnership with the University of Ottawa. Additional financial support was provided by the Natural Sciences and Engineering Research Council of Canada (NSERC) to D. Krewski, who holds the NSERC Chair in Risk Science at the University of Ottawa. C.C. Willhite, N.A. Karyakina, F. Momoli, and N. Yenugadhati were compensated by RSI for their contributions to the review. I. Arnold, T. Wisniewski and R. Yokel received no compensation from RSI for their contributions to this work. The authors, whose affiliations are shown on the title page, had sole responsibility for preparation of this paper, including determining the strategy for reviewing the scientific literature summarized in this article, synthesizing the findings, and drawing conclusions. Scientists associated with IAI/ARC were given the opportunity to review and offer technical comments on the paper, prior to submission to Critical Reviews in Toxicology. I. Arnold serves as a consultant to the International Aluminium Institute. None of the authors have appeared before regulatory agencies on behalf of the sponsors, or appeared as experts in legal proceedings concerning matters reviewed in this paper. The scientific opinions and conclusions expressed in the paper are exclusively those of the authors, and are independent of the sources of financial support. HHS Public Access Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptThe present review represents a systematic examination of the peer-reviewed literature on the adverse health effects of Al materials published since a previous critical evaluation compiled by Krewski et al. (2007). The scientific literature on the adverse health effects of Al is extensive. Health risk assessments for Al must take into account individual co-factors (e.g., age, renal function, diet, gastric pH). Conclusions from the current review point to the need for refinement of the PTWI, reduction of Al contamination in PN solutions, justification for routine addition of Al to vaccines, and harmonization of OELs for Al substances.

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Memantine prevents aluminum-induced cognitive deficit in rats

Cited by 18 publications

References 60 publications

Docosahexaenoic Acid (DHA), Vitamin D3, and Probiotics Supplementation Improve Memory, Glial Reactivity, and Oxidative Stress Biomarkers in an Aluminum-Induced Cognitive Impairment Rat Model

Docosahexaenoic Acid (DHA), Vitamin D3, and Probiotics Supplementation Improve Memory, Glial Reactivity, and Oxidative Stress Biomarkers in an Aluminum-Induced Cognitive Impairment Rat Model

Memantine can relieve the neuronal impairment caused by neurotropic virus infection

Systematic review of potential health risks posed by pharmaceutical, occupational and consumer exposures to metallic and nanoscale aluminum, aluminum oxides, aluminum hydroxide and its soluble salts

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