Magnesium Protects Cognitive Functions and Synaptic Plasticity in Streptozotocin-Induced Sporadic Alzheimer’s Model

Abstract

Alzheimer’s disease (AD) is characterized by profound synapse loss and impairments of learning and memory. Magnesium affects many biochemical mechanisms that are vital for neuronal properties and synaptic plasticity. Recent studies have demonstrated that the serum and brain magnesium levels are decreased in AD patients; however, the exact role of magnesium in AD pathogenesis remains unclear. Here, we found that the intraperitoneal administration of magnesium sulfate increased the brain magnesium levels and protected learning and memory capacities in streptozotocin-induced sporadic AD model rats. We also found that magnesium sulfate reversed impairments in long-term potentiation (LTP), dendritic abnormalities, and the impaired recruitment of synaptic proteins. Magnesium sulfate treatment also decreased tau hyperphosphorylation by increasing the inhibitory phosphorylation of GSK-3β at serine 9, thereby increasing the activity of Akt at Ser473 and PI3K at Tyr458/199, and improving insulin sensitivity. We conclude that magnesium treatment protects cognitive function and synaptic plasticity by inhibiting GSK-3β in sporadic AD model rats, which suggests a potential role for magnesium in AD therapy.

Sodium selenate regulates the brain ionome in a transgenic mouse model of Alzheimer’s disease

“…It was reported that Mg has neuroprotective effect, whose deficit in the serum or brain might be a risk factor for AD50515253. To date, the relationship between V or Cr and AD is not clear.…”

Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a streptozotocin model of Alzheimer’s disease

“…Synaptic dysfunctions in animal models of Alzheimer's disease have been well addressed in transgenic models (Chakroborty et al, 2012;Sancheti et al, 2013;Clark et al, 2015). Additionally, Xu et al (2014) have reported that icv-STZ decreases the dendritic spine density, which was in turn associated with alterations in spatial memory and hippocampal LTP in vitro. As our study differentiates between affected LTP and unaffected PPF, we suggest that both the icv-STZ model and human sAD may present postsynaptic -rather than presynaptic -plasticity dysfunctions.…”

Markers of cognitive impairment in patients with type 2 diabetes

“…The mechanisms by which Mg Brought to you by | MIT Libraries Authenticated Download Date | 5/13/18 3:54 AM might protect from cognitive impairment are not entirely clear. Some in vitro and animal studies have shown that Mg is associated with reduced production and increased degradation of toxic hyperphosphorylated protein tau, modulation of amyloid-beta protein precursor processing, reduction of neuro-inflammation and protection of synaptic plasticity (30)(31)(32)(33). T2D often seems to be accompanied by alteration of Mg status, with reduction of serum and intracellular free Mg levels, which is associated with decreased insulin sensitivity (34).…”