md-medicaldata

Authors

 

Bojan Batinić¹, Vesna Pešić<sup>1

1</sup>Katedra za fiziologiju, Farmaceutski fakultet, Univerzitet u Beogradu, Vojvode Stepe 450, 11 221 Beograd, Srbija

 

UDK: 616.8-085.3:546.46
615.3.015:546.46

The paper was received / Rad primljen: 02.01.2019.

Accepted / Rad prihvaćen: 24.01.2019.

 

Correspondence to:

Bojan Batinić
Katedra za fiziologiju, Farmaceutski fakultet, Univerzitet u Beogradu
Adresa: Vojvode Stepe 450, 11221 Beograd, Srbija
Tel: +381 63 272 061
e-mail: bojan.batinic@pharmacy.bg.ac.rs

 

 

Sažetak

 

Oštećenja kognitivnih funkcija su u mnogim neurološkim oboljenjima povezana sa hroničnim ili akutnim deficitom magnezijuma u nervnom sistemu. Terapijski potencijal magnezijuma u unapređenju kognitivnih funkcija ispitivan je najviše u modelima Alchajmerove bolesti (AB), traumatične povrede mozga i starenja, ali i kod zdravih životinja. Povećanje koncentracije ovog bioelementa u mozgu eksperimentalnih životinja postignuto je primenom različitih jedinjenja poput Mg-treonata, Mg-sulfata i Mg-hlorida. Centralni efekti magnezijuma, opisani u pretkliničkim studijama, obuhvataju poboljšanje performansi u bihejvioralnim testovima učenja i memorije, kao i morfološke i funkcionalne promene na nivou neurona. U modelu AB, tretman magnezijumom je prevenirao pojavu amiloidnih plakova, redukovao gubitak neuronskih sinapsi i abnormalnosti dendrita. U modelu starenja doveo je do rekonfiguracije i povećanja funkcionalnosti sinapsi na pre- i postsinaptičkom nivou, kroz regulaciju oslobađanja neurotransmitera i ekspresije NMDA receptora, što se povezuje sa poboljšanjem memorije. I pored afirmativnih nalaza u pretkliničkim studijama, neuroprotektivni i prokognitivni efekti magnezijuma još uvek nisu ispitivani kod AB pacijenata ili zdravih subjekata sa kognitivnim oštećenjima.

 

 

Ključne reči:

Magnezijum, memorija, učenje, NMDA receptor

 

 

Abstract

 

Cognitive deficits in many neurological disorders are related to a chronic or acute lack of magnesium in the central nervous system. Therapeutic potential of magnesium in the improvement of cognitive functions has been investigated mostly in animal models of Alzheimer’s disease (AD), traumatic brain injury and aging, as well as in healthy animals. An increase of magnesium brain concentration in experimental animals has been achieved using different compounds such as Mg-threonate, Mg-sulfate and Mg-chloride. Central effects of magnesium, described in preclinical studies, include improvement of performances in different behavioral tests of learning and memory, as well as morphological and functional changes in neurons. In a model of AD, magnesium prevented the development of amyloid plaques, reduced the loss of neuronal synapses and diminished dendrite abnormalities. In aged animals, magnesium induced a reconfiguration of synapses and their functional improvements, by regulating the neurotransmitter release and the expression of NMDA receptors, which is related to memory improvement. Although preclinical studies provided affirmative results, the neuroprotective and procognitive effects of magnesium have not yet been investigated in AD patients or healthy humans with cognitive impairments.

 

Key words:

Magnesium, memory, learning, NMDA receptors

 

 

 

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PDF Batinić B. and Pešić V. • MD-Medical Data 2019;11(1): 023-027