Brain aluminum, magnesium and phosphorus contents of control and Alzheimer-diseased patients

Andrási, Erzsébet; Páli, N.; Molnár, Zsuzsa; Kösel, S.

doi:10.3233/jad-2005-7402

Cited by 123 publications

(83 citation statements)

References 34 publications

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“…If impairment in cognitive functions in AD patients is mainly caused by synapse failure/loss (Selkoe, 2002), it is relevant to determine whether elevation of brain magnesium could still be effective under AD-like pathological conditions. Furthermore, brain magnesium levels (Andrási et al, 2005) and serum Mg 2ϩ concentrations (Barbagallo et al, 2011) appear to be significantly lower in AD patients compared with age-matched normal subjects. If this is the case, then simply restoring brain magnesium might beneficiate AD patients.…”

Section: Introductionmentioning

confidence: 99%

Elevation of Brain Magnesium Prevents and Reverses Cognitive Deficits and Synaptic Loss in Alzheimer's Disease Mouse Model

Jia

Liu

et al. 2013

J. Neurosci.

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Profound synapse loss is one of the major pathological hallmarks associated with Alzheimer's disease (AD) and might underlie memory impairment. Our previous work demonstrated that the magnesium ion is a critical factor in controlling synapse density/plasticity. Here, we investigated whether elevation of brain magnesium by the use of a recently developed compound, magnesium-L-threonate (MgT), can ameliorate the AD-like pathologies and cognitive deficits in the APPswe/PS1dE9 mice, a transgenic (Tg) mouse model of AD. MgT treatment reduced A␤ plaque and prevented synapse loss and memory decline in the Tg mice. Strikingly, MgT treatment was effective even when given to the mice at the end stage of their AD-like pathological progression. To explore how elevation of brain magnesium ameliorates the AD-like pathologies in the brains of Tg mice, we studied molecules critical for APP metabolism and signaling pathways implicated in synaptic plasticity/density. In the Tg mice, the NMDAR/CREB/BDNF signaling was downregulated, whereas calpain/ calcineurin/Cdk5 neurodegenerative signaling and ␤-secretase (BACE1) expression were upregulated. MgT treatment prevented the impairment of these signaling pathways, stabilized BACE1 expression, and reduced soluble APP␤ and ␤-C-terminal fragments in the Tg mice. At the molecular level, elevation of extracellular magnesium prevented the high-A␤-induced reductions in synaptic NMDARs by preventing calcineurin overactivation in hippocampal slices. Correlation studies suggested that the protection of NMDAR signaling might underlie the stabilization of BACE1 expression. Our results suggest that elevation of brain magnesium exerts substantial synaptoprotective effects in a mouse model of AD and may have therapeutic potential for treating AD in humans.

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Section: Introductionmentioning

confidence: 99%

Elevation of Brain Magnesium Prevents and Reverses Cognitive Deficits and Synaptic Loss in Alzheimer's Disease Mouse Model

Jia

Liu

et al. 2013

J. Neurosci.

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“…Atom absorption spectrography revealed that Al content is (3.6±2.9) mg/g dry weight in AD brain, higher than the content (1.8±0.8) mg/g in normal human brain. Brain cell degeneration can be produced when Al level is above 4 mg/g [21,22] . Free Al may enter the septal nuclei and amygdala, where Al is prone to form deposits [23,24] .…”

Section: Combined Administration Of D-gal and Al For 8 And 10mentioning

confidence: 99%

Combined administration of D-galactose and aluminium induces Alzheimerlike lesions in brain

et al. 2011

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“…An epidemiological study supported the hypothesis of an association between chronic exposure to aluminium and the incidence of AD (7); however, this has yet to be elucidated. Additionally it has been revealed that levels of aluminium are elevated in the brains of patients with AD (8).…”

Section: Introductionmentioning

confidence: 99%

Memory-enhancing effect of aspirin is mediated through opioid system modulation in an AlCl3-induced neurotoxicity mouse model

Rizwan

Idrees

Ashraf

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Neurodegenerative disorders such as Alzheimer's disease (AD) are multifaceted and there are currently a limited number of therapeutic strategies available to treat them. Aspirin is known to act on multiple therapeutic targets and is a successful anti-inflammatory agent in various tissues. The present study aimed to ascertain the performance of aspirin when employed as a therapeutic agent to treat neurodegeneration on novel targets, including opioid system genes, in an AlCl 3 -induced neurotoxicity mouse model. The effects of two doses of aspirin (5 and 20 mg/kg aspirin for 12 days) were investigated in an AlCl 3 -induced neurotoxicity mouse model (150 mg/kg AlCl 3 for 12 days). Neurological improvements were assessed through different behavioral tests and the effects of aspirin on opioid system gene expression levels were assessed by reverse transcription-polymerase chain reaction. Both doses resulted in improvements in cognitive behavior. A 5 mg/kg dose of aspirin was revealed to be effective for spatial memory improvement (7.14±0.84 sec), whilst a 20 mg/kg dose was superior for improving extinction learning (7.63±4.04%). Aspirin (5 mg/kg) also significantly improved contextual memory (48.05±10.6%) when compared with the AlCl 3 -treated group (1.49±0.62%; P<0.001). Aspirin was also observed to significantly decrease δ-opioid receptor expression in the cortex (1.09±0.08 and 1.27±0.08, respectively) at both doses (5 and 20 mg/kg) when compared with the AlCl 3 -treated group (3.69±1.43; P<0.05). Furthermore, aspirin at 5 mg/kg significantly reduced expression of prodynorphin in the cortex (0.57±0.20) when compared with the AlCl 3 -treated group (1.95±0.84; P<0.05). Notably, the effect of aspirin was significant in the cortex but not in the hippocampus. In summary, aspirin was effective in ameliorating the AD-like symptoms via the modulation of opioid systems. However, additional studies are required to determine the long term effects of aspirin on such conditions.

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Brain aluminum, magnesium and phosphorus contents of control and Alzheimer-diseased patients

Cited by 123 publications

References 34 publications

Elevation of Brain Magnesium Prevents and Reverses Cognitive Deficits and Synaptic Loss in Alzheimer's Disease Mouse Model

Elevation of Brain Magnesium Prevents and Reverses Cognitive Deficits and Synaptic Loss in Alzheimer's Disease Mouse Model

Combined administration of D-galactose and aluminium induces Alzheimerlike lesions in brain

Memory-enhancing effect of aspirin is mediated through opioid system modulation in an AlCl3-induced neurotoxicity mouse model

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