Can the Controversy of the Role of Aluminum in Alzheimer's Disease Be Resolved? What Are the Suggested Approaches to This Controversy and Methodological Issues to Be Considered?

Savory, Christopher Exley John

doi:10.1080/009841096161104

Cited by 138 publications

(1 citation statement)

References 68 publications

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“…In our study (Fig. 5), upregulation was observed in hippocampal mRNA gene expression of Aβ protein among Alinduced untreated animals compared to normal control, an effect that could be connected to the neurotoxic effects of Al (Savory et al 1996). Also, Al has been reported to in uence Aβ neurotoxicity through an indirect in uence on its enzymatic degradation in peripheral tissues (Sanajou et al 2002), as well as the formation and proliferation of ROS in a reaction that is activated by the release/presence of Fe 2+ or Cu 2+ (Exley et al 1993).…”

Section: Discussionsupporting

confidence: 57%

Neuromodulatory effects of caffeine, vanillin and their combination via the assessment of hippocampal purinergic enzymes and expressions of cholinergic, eNOS, GABA receptor, amyloid protein and histomorphological status of AlCl3-induced Alzheimer’s disease in adult male Wistar rats

Afolabi,

Jaiyesimi,

Olasehinde

et al. 2023

Preprint

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The neurotoxic properties of aluminum (Al) have been associated with Alzheimer's disease (AD) development. Consequently, there has been an increasing interest in exploring how bioactive compounds from functional foods can mitigate the detrimental impact of this redox metal in AD. Hence, this study evaluated neuromodulatory effects of caffeine, vanillin and their combination on some hippocampal biochemical parameters in AlCl3-induced AD. Thirty-six (36) adult male Wistar rats (150–200 g) were randomly divided into 6 treatment groups of 6 rats each. Animals were exposed to AlCl3 (100 mg/kg body weight, bw) orally at a single dose to induce AD. Experimental AlCl3-induced animals were administered with 50 mg/kg bw caffeine, vanillin and their combination for 21 days with donepezil (10 mg/kg bw) as control. However, following the 21 days treatment with 50 mg/kg caffeine, vanillin and their combination, a noticeable significant (p < 0.05) decrease was observed in the hippocampal ENTPDase activity with a concomitant increase significantly (p < 0.05) in eNTDase activity, respectively. Also, a significant (p < 0.05) reduction was evident in the hippocampal relative mRNA gene levels of eNOS, AChE and β-amyloid protein with no significant difference in the expression of GABA receptor protein in some treatment groups compared to untreated AlCl3-induced control group. Similarly, hippocampal architecture revealed restoration of dentate gyrus with an increased granular cell counts after the 21 days of treatment. Thus, according to our findings, the ability of caffeine, vanillin and their combination to modulate hippocampal purinergic system and expressions of some vital proteins in AlCl3-induced AD could possibly be a potential therapy in the management of AD.

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Section: Discussionsupporting

confidence: 57%

Neuromodulatory effects of caffeine, vanillin and their combination via the assessment of hippocampal purinergic enzymes and expressions of cholinergic, eNOS, GABA receptor, amyloid protein and histomorphological status of AlCl3-induced Alzheimer’s disease in adult male Wistar rats

Afolabi,

Jaiyesimi,

Olasehinde

et al. 2023

Preprint

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Neurobehavioral performance in aluminum welders

et al. 2000

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A unifying hypothesis of Alzheimer's disease. III. Risk factors

Heininger

2000

Hum. Psychopharmacol. Clin. Exp.

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Normal ageing and Alzheimer's disease (AD) have many features in common and, in many respects, both conditions only differ by quantitative criteria. A variety of genetic, medical and environmental factors modulate the ageing-related processes leading the brain into the devastation of AD. In accordance with the concept that AD is a metabolic disease, these risk factors deteriorate the homeostasis of the Ca(2+)-energy-redox triangle and disrupt the cerebral reserve capacity under metabolic stress. The major genetic risk factors (APP and presenilin mutations, Down's syndrome, apolipoprotein E4) are associated with a compromise of the homeostatic triangle. The pathophysiological processes leading to this vulnerability remain elusive at present, while mitochondrial mutations can be plausibly integrated into the metabolic scenario. The metabolic leitmotif is particularly evident with medical risk factors which are associated with an impaired cerebral perfusion, such as cerebrovascular diseases including stroke, cardiovascular diseases, hypo- and hypertension. Traumatic brain injury represents another example due to the persistent metabolic stress following the acute event. Thyroid diseases have detrimental sequela for cerebral metabolism as well. Furthermore, major depression and presumably chronic stress endanger susceptible brain areas mediated by a host of hormonal imbalances, particularly the HPA-axis dysregulation. Sociocultural and lifestyle factors like education, physical activity, diet and smoking may also modulate the individual risk affecting both reserve capacity and vulnerability. The pathophysiological relevance of trace metals, including aluminum and iron, is highly controversial; at any rate, they may adversely affect cellular defences, antioxidant competence in particular. The relative contribution of these factors, however, is as individual as the pattern of the factors. In familial AD, the genetic factors clearly drive the sequence of events. A strong interaction of fat metabolism and apoE polymorphism is suggested by intercultural epidemiological findings. In cultures, less plagued by the 'blessings' of the 'cafeteria diet-sedentary' Western lifestyle, apoE4 appears to be not a risk factor for AD. This intriguing evidence suggests that, analogous to cardiovascular diseases, apoE4 requires a hyperlipidaemic lifestyle to manifest as AD risk factor. Overall, the etiology of AD is a key paradigm for a gene-environment interaction. Copyright 2000 John Wiley & Sons, Ltd.

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Can the Controversy of the Role of Aluminum in Alzheimer's Disease Be Resolved? What Are the Suggested Approaches to This Controversy and Methodological Issues to Be Considered?

Cited by 138 publications

References 68 publications

Neuromodulatory effects of caffeine, vanillin and their combination via the assessment of hippocampal purinergic enzymes and expressions of cholinergic, eNOS, GABA receptor, amyloid protein and histomorphological status of AlCl3-induced Alzheimer’s disease in adult male Wistar rats

Neuromodulatory effects of caffeine, vanillin and their combination via the assessment of hippocampal purinergic enzymes and expressions of cholinergic, eNOS, GABA receptor, amyloid protein and histomorphological status of AlCl3-induced Alzheimer’s disease in adult male Wistar rats

Neurobehavioral performance in aluminum welders

A unifying hypothesis of Alzheimer's disease. III. Risk factors

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