MAGNÉSIO L TREONATO (MgT) 98%

Forma de magnésio com maior efetividade no Sistema Nervoso Central (SNC)

CAS: 778571-57-6
DCB: N/A
Fórmula Molecular: C8H14MgO10
Peso Molecular: 294,5 g/mol
Teor: 98%

Posologia sugerida:

Usual: 500 mg/dia. 1 vez ao dia a noite.

Máximo: 1.500mg

Indicações

• Melhora memória de curto e longo prazo

• Saúde cognitiva
• Melhora aprendizado;
• Melhora da densidade e da função neuronal
• Aumenta intensidade das sinapses
• Eficaz doença de Alzheimer - melhora memória recente
• Coadjuvante em doenças neurodegenerativas
• Reduz ansiedade e estresse
• Benefício pessoas que sofrem de depressão, síndrome do pânico
• Melhora na qualidade do sono
• Melhora captação de glicose

Sal magnésio sob a forma de ácido L- treônico, metabólico natural da vitamina C, facilita
biodisponibilidade

Forma moderna para elevar a absorção de magnésio

Principais benefícios

• Quando o Magnésio está associado ao agente de quelação L-treonato – um metabólito

da vitamina C - a biodisponibilidade cerebral é significativamente melhorada,
beneficiando assim as conexões sinápticas e a sinalização neuronal. Dessa forma, o
Magnésio L Treonato melhora a função cognitiva, a aprendizagem e os processos
mnemônicos.

• MGT possui características que o permite ultrapassar a barreira hematoencefálica com mais
facilidade.

Magnésio é o quarto mineral mais prevalente do corpo humano, sendo de grande importância
para diversos processos vitais como contração muscular, formação óssea, metabolismo
energético, regulação do humor e do sono e ainda como cofator para absorção de nutrientes,
tal como a vitamina D. Magnésio é um cofator de diversas reações químicas.
Além disso, o Magnésio desempenha um papel essencial na função cerebral, contudo, por muitas
vezes sua distribuição para este tecido é limitada.

Um mineral que, ao longo das últimas décadas, tem sido considerado de elevada importância em
várias lesões neurológicas e que interage com outros micronutrientes para manter e promover o
desempenho da função cognitiva, tal como a aprendizagem (Huskisson et al., 2007).

Desempenha várias funções fisiológicas e homeostáticas, como a regulação do tônus vascular, e

atua como um antagonista do cálcio, levando ao bloqueio não competitivo dos receptores
NMDA no cérebro, controlando assim a sua abertura, que é fundamental para a plasticidade
sináptica. (Basheer et al., 2015).

Em relação à plasticidade sináptica, o magnésio é um regulador positivo. O aumento da sua

concentração no fluido extracelular, dentro dos níveis fisiológicos, conduz a uma melhoria
permanente da plasticidade sináptica em redes de neurônios do hipocampo, cultivados in vitro.
Em publicações recentes, tem-se demonstrado os efeitos positivos de Magnésio L-treonato (MgT),
nos quais estão incluídos a melhoria da memória e da aprendizagem. No geral, a suplementação
de magnésio foi eficaz na correção de deficiências cognitivas moderadas (Moncayo et al., 2015).
Permite assim um aumento dos níveis de magnésio no cérebro face aos suplementos
convencionais, elevando a densidade e plasticidade sináptica, resultando em melhorias da
memória e cognição. Investigadores do MIT testaram a memória de trabalho espacial em modelos
experimentais e verificaram que, no caso de suspender o MgT, a capacidade de memória
decresce para a linha de base inicial, o que comprova a sua importância (Alessio, 2012).

Mecanismo Ação

Magnésio L-treonato aumenta significativamente a concentração de magnésio no cérebro

fazendo com que a densidade das sinapses às ligações entre os neurônios, essenciais à
capacidade de aprendizagem e de memorização dependente da idade, conduzam a melhora
da aprendizagem e memória de trabalho, bem como da memória a curto e longo prazo. Assim,
a utilização do Magnésio L-treonato eleva os níveis de magnésio no cérebro, a densidade e a
plasticidade das sinapses e melhora as capacidades cognitivas a ela associadas.

Contra indicações

Insuficiência renal, níveis de ureia e creatina elevados, diálise

Sugestões Formulações

Magnésio L treonato..........500mg
Lion’s mane........................ 250mg
Posologia: 1 vez ao dia, à noite.

Estudos clínicos

• Prevention of cognitive deficits in Alzheimer’s mouse model by elevating brain magnesium

Memory functions decline with age, and severely deteriorate during Alzheimer’s disease (AD).
Several studies suggest that dietary/environmental factors can reduce the prevalence of AD in
humans. Magnesium is essential for maintaining normal body and brain functions. Here we show
that increasing brain magnesium, using a newly developed magnesium compound (magnesium-
L-threonate, MgT), prevents cognitive deficits and pathological changes in transgenic mice co-
expressing familial AD-linked APP and PS1 variants that mimics the pathological and behavioral
changes of human AD (AD mice). In intact mice, brain Mg content was found to be the lowest
among all tissues tested; long-term MgT-treatment significantly elevated Mg levels in brain, and was
associated with markedly improved cognitive function. In AD mice, learning and memory abilities
are seriously impaired by 7 months, and completely deteriorate at 15 months. Strikingly, MgT-
treatment was effective in preventing such severe learning and memory deterioration during the
entire course of AD progression. At the cellular level, MgT-treatment reduced amyloid deposition in
hippocampus and frontal cortex, and prevented synapse loss in the dentate gyrus (DG) and CA1
areas. The degree of memory improvement was strongly correlated with the protection of synapse
loss, but did not correlate with the reduction of Aβ plaque. Thus, increased brain Mg might block
Aβ-induced synaptic dysfunction. Since AD patients already have Mg deficiency, increase in brain
Mg may represent a new strategy for prevention and amelioration of AD.

• Enhancement of learning and memory by elevating brain magnesium

Learning and memory are fundamental brain functions affected by dietary and environmental
factors. Here, we show that increasing brain magnesium using a newly developed magnesium
compound (magnesium-L-threonate, MgT) leads to the enhancement of learning abilities, working
memory, and short- and long-term memory in rats. The pattern completion ability was also improved
in aged rats. MgT-treated rats had higher density of synaptophysin- /synaptobrevin-positive puncta
in DG and CA1 subregions of hippocampus that were correlated with memory improvement.
Functionally, magnesium increased the number of functional presynaptic release sites, while it
reduced their release probability. The resultant synaptic reconfiguration enabled selective
enhancement of synaptic transmission for burst inputs. Coupled with concurrent upregulation of
NR2B-containing NMDA receptors and its downstream signaling, synaptic plasticity induced by
correlated inputs was enhanced. Our findings suggest that an increase in brain magnesium
enhances both short-term synaptic facilitation and long-term potentiation and improves learning
and memory functions.

• Magnesium L-threonate Prevents and Restores Memory Deficits Associated with Neuropathic
Pain by Inhibition of TNF-α

Background: Clinical studies have shown that about two-thirds of patients with chronic pain suffer
from short-term memory (STM) deficits and an effective drug for treatment of the neurological
disorder is lacking at present. Objective: We tested whether chronic oral application of magnesium
L-threonate (MgT), which has been shown to improve memory in normal and aging animals by
elevating Mg2+ in the brain, could prevent or restore the STM deficits induced by spared nerve injury
(SNI), an animal model of chronic neuropathic pain. The mechanisms underlying the effect of MgT
on STM deficits were also investigated. Study Design: The experiments were conducted in a random
and double-blind fashion in adult male rats. MgT was administrated via drinking water at a dose of
609 mg/kg/d for 2 weeks, starting either one week before SNI (preventative group) or one week
after SNI (therapeutic group), and water without the drug served as control. Methods: STM was
accessed with a novel object recognition test (NORT), followed by recording of long-term
potentiation (LTP) in the hippocampus in vivo and the measurement of the expression. of tumor
necrosis factor-α (TNF-α) with Western Blot or Immunohistochemistrical staining. α-amino-3-hydroxy-
5-methyl4-isoxazole-propionic acid (AMPA) and N-methyl-D-aspartic acid (NMDA) receptor
(NMDAR) currents were recorded with patch clamp in CA1 neurons in acute and cultured
hippocampal slices. Result: We found that chronic oral application of MgT was able to prevent and
restore the deficits of STM and of LTP at CA3-CA1 synapses in the hippocampus induced by SNI.
Furthermore, both preventative and therapeutic chronic oral application of MgT blocked the up-
regulation of TNF-α in the hippocampus, which has been previously shown to be critical for memory
deficits. SNI reduced NMDAR current and the effect was dramatically attenuated by elevating
extracelular Mg2+ concentration ([Mg2+]o). In cultured hippocampal slices, chronic application of
recombinant rat TNF-α (rrTNF-α) for 3 days reduced NMDAR current in a concentration-dependent
manner and the effect was again blocked by elevating [Mg2+]o. Limitations: We showed that oral
application of MgT inhibited the over-expression of TNF-α and rescued the dysfunction of the
NMDAR, but the causal relationship between them remains elusive. Conclusions: Our data
suggested that oral application of MgT was able to prevent and restore the STM deficits in an animal
model of chronic neuropathic pain by reversing the dysfunction of the NMDAR, and normalization
of TNF-α expression may play a role in the effect. Oral application of MgT may be a simple and
potent means for handling this form of memory deficit.

Referências bibliográficas

LIU G. Prevention of cognitive deficits in Alzheimer’s mouse model by elevating brain magnesium. Mol Neurodegener. V. 7, nº1. 2012.
Disponível em:< http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3287610/>.

SLUTSKY I.; ABUMARIA N.; WU L.J.; HUANG C.; ZHANG L.; LI B.; ZHAO X.; GOVINDARAJAN A.; ZHAO M.G.; ZHUO M.; TONEGAWA S.; LIU G.
Enhancement of learning and memory by elevating brain magnesium. Neuron. V.65, n°2, p.165-77. Jan; 2010. Disponível em:<
http://www.ncbi.nlm.nih.gov/pubmed/20152124>.

Jun Wang, Yong Liu, Li-Jun Zhou, Ying Wu, Fei Li, Kai-Feng Shen, Rui-Ping Pang, Xu-Hong Wei, Yong-Yong Li, and Xian-Guo Liu, “Magnesium
Lthreonate Prevents and Restores Memory Deficits Associated with Neuropathic Pain by Inhibition of TNF-α”; Pain Physician 2013; 16:E563-
E575.

Wei Li, Jia Yu, Yong Liu, Xiaojie Huang, Nashat Abumaria, Ying Zhu, Xian Huang, Wenxiang Xiong, Chi Ren, Xian-Guo Liu, Dehua Chui and
Guosong Liu. “Elevation of brain magnesium prevents synaptic loss and reverses cognitive deficits in Alzheimer’s disease mouse model”;
Molecular Brain 2014, 7:65.

Qifeng Sun, Jason G. Weinger, Fei Mao, Guosong Liu. “Regulation of Structural and Functional Synapse Density by L-Threonate Through
Modulation of Intraneural Magnesium Concentration”, Neuropharmacology 108 (2016) 426

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