Magnesium ions show promise in slowing progression of
Alzheimer’s disease in mice

Magnesium ions may slow the progression of the disease by
disrupting the development of amyloid plaques, research suggests

In mouse models Alzheimer’s disease,
oral administration of magnesium-L-threonate (MgT) alleviated cognitive
decline, scientists report in a new article.

New research published in the December 2015 issue
of The FASEB Journal, shows that in mouse models of the disease oral
administration of magnesium-L-threonate (MgT) alleviated cognitive decline by
suppressing the Aβ deposition in amyloid plaques in an APH-1α/1β-dependent
manner. Although questions still remain about how MgT permeates the blood-brain
barrier, the work suggests that scientists may have found the key to a new
series of Alzheimer’s disease treatments. Specifically, they show that
magnesium ions target pharynx defective (APH)-APH-1α/1β-suppressing the A?
deposition in amyloid plaques in an anterior pharynx defective
(APH)-APH-1α/1β-dependent manner.

“We hope that our findings will help improve
clinical practice pertinent to the optimal administration of Mg2+ for delaying
or even preventing the onset of AD,” said Pu Wang, Ph.D., a researcher
involved in the work from the Department of Life Science and Health at
Shenyang, Liaoning, China. “Moreover, we hope to extend our experimental
models to other disorders such as severe craniocerebral injury, bronchial
asthma, chronic pulmonary heart disease, arrhythmia and myocardial necrosis,
etc. and identify more targets of Mg2+ and strategies for treating these
disorders.”

To make this discovery, Wang and colleagues used two
groups of mice. The first group consisted of normal mice. The second group
consisted of mice overexpressing a gene that enhances the expression of
APH-APH-1α/1β and the production of Aβ, while also decreasing the Mg2+ influx
in the brain, especially in cerebrospinal fluid. When researchers restored Mg2+
in the cerebrospinal fluid of the genetically modified mice, the highly induced
APH-APH-1α/1β expression was inhibited, which resulted in alleviating Aβ
aggregation and cognitive decline. Although the researchers did not find any
direct evidence showing that MgT was able to penetrate the blood brain barrier,
their findings showed elevated levels of Mg2+ in the brains of the genetically
modified mice–sufficient for inhibiting the development of Alzheimer’s
disease.

“The good news about this work is that if it holds
up in humans, magnesium is a common element that is readily available,”
said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal.
“The bad news, of course, is that what works in mice does not always turn
out so well in people. At the same time, even if magnesium ions do not work out
for people with Alzheimer’s, this report will help researchers learn how to
slow the development amyloid plaques, a hallmark of the disease.”

Journal Reference:

X. Yu, P.-P. Guan, J.-W. Guo, Y. Wang, L.-L. Cao, G.-B.
Xu, K. Konstantopoulos, Z.-Y. Wang, P. Wang. By suppressing the expression
of anterior pharynx-defective-1  and -1  and inhibiting the aggregation
of  -amyloid protein, magnesium ions inhibit the cognitive decline of
amyloid precursor protein/presenilin 1 transgenic mice. The FASEB Journal,
2015; 29 (12): 5044 DOI: 10.1096/fj.15-275578

Normal
0

false
false
false

EN-US
X-NONE
X-NONE

/* Style Definitions */
table.MsoNormalTable
{mso-style-name:”Table Normal”;
mso-tstyle-rowband-size:0;
mso-tstyle-colband-size:0;
mso-style-noshow:yes;
mso-style-priority:99;
mso-style-parent:””;
mso-padding-alt:0in 5.4pt 0in 5.4pt;
mso-para-margin:0in;
mso-para-margin-bottom:.0001pt;
mso-pagination:widow-orphan;
font-size:11.0pt;
font-family:”Calibri”,sans-serif;
mso-ascii-font-family:Calibri;
mso-ascii-theme-font:minor-latin;
mso-hansi-font-family:Calibri;
mso-hansi-theme-font:minor-latin;}