By a News Reporter-Staff News Editor at Pain & Central Nervous System Week -- Current study results on Neurodegenerative Diseases have been published. According to news reporting originating from Austin, Texas, by NewsRx correspondents, research stated, "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."
Our news editors obtained a quote from the research from the University of Texas, "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 beta 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 beta-secretase (BACE1) expression were upregulated. MgT treatment prevented the impairment of these signaling pathways, stabilized BACE1 expression, and reduced soluble APP beta and beta-C-terminal fragments in the Tg mice. At the molecular level, elevation of extracellular magnesium prevented the high-A beta-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."
According to the news editors, the research concluded: "Our results suggest that elevation of brain magnesium exerts substantial synap-toprotective effects in a mouse model of AD and may have therapeutic potential for treating AD in humans."
For more information on this research see: Elevation of Brain Magnesium Prevents and Reverses Cognitive Deficits and Synaptic Loss in Alzheimer's Disease Mouse Model. Journal of Neuroscience, 2013;33(19):8423-8441. Journal of Neuroscience can be contacted at: Soc Neuroscience, 11 Dupont Circle, NW, Ste 500, Washington, DC 20036, USA. (Society for Neuroscience - www.sfn.org/; Journal of Neuroscience - www.sfn.org/index.aspx?pagename=JournalOfNeuroscience)
The news editors report that additional information may be obtained by contacting W. Li, Univ Texas Austin, Center Learning & Memory, Austin, TX 78712, United States (see also Neurodegenerative Diseases).
Keywords for this news article include: Texas, Austin, Dementia, Magnesium, Treatment, Tauopathies, Light Metals, Therapeutics, United States, Brain Diseases, Alzheimer Disease, North and Central America, Neurodegenerative Diseases, Central Nervous System Diseases
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