Skip to main content Accessibility help
×
Hostname: page-component-76fb5796d-skm99 Total loading time: 0 Render date: 2024-04-27T22:26:14.717Z Has data issue: false hasContentIssue false

Chapter 17 - Magnesium in Parkinson's disease: an update in clinical and basic aspects

from Section 2 - Magnesium in Neurological Diseases

Published online by Cambridge University Press:  05 June 2012

Kiyomitsu Oyanagi
Affiliation:
Department of Brain Disease Research, Shinshu University School of Medicine, Matsumoto, Nagano 390-8621, Japan
Tomoyo Hashimot
Affiliation:
Department of Brain Disease Research, Shinshu University School of Medicine, Matsumoto, Nagano 390-8621, Japan
Robert Vink
Affiliation:
University of Adelaide
Mihai Nechifor
Affiliation:
University of Medicine and Pharmacy, Iasi, Romania
Get access

Summary

Abstract

Magnesium (Mg) is essential for cell functions such as transport of calcium and potassium ions, and modulates signal transduction, energy metabolism, and cell proliferation. Several studies elucidated a reduced concentration of Mg in patients with Parkinson's disease (PD), and experimentally, severe loss of dopaminergic neurons exclusively in the substantia nigra in 1-year-old rats that had been subjected to continuously low Mg intake (one-fifth of the normal level) over generations. A study conducted by the authors revealed a significant and striking effect of Mg to prevent neurite and neuron pathology, and also to ameliorate neurite pathology in a rat Parkinson disease (PD) model involving culture of ventral mesencephalic-striatal cells with 1-methyl-4-phenylpyridinium (MPP+). Mg is expected to prevent and ameriolate Parkinson's disease in cases where it would be able to cross into the brain in a suitable way.

Introduction

Parkinson's disease (PD) is a neurodegenerative disease occurring in middle-aged and aged humans characterized by clinical symptoms including tremor and rigidity (Parkinson, 1817). It has been reported that almost 90% of the patients are sporadic and 10% are familial. Sporadic PD shows neuropathological features involving the appearance of Lewy bodies (Lewy, 1912; Tretiakoff, 1919) and loss of neurons in the substantia nigra (Figures 1 and 2) and substantia innominata.

Type
Chapter
Information
Publisher: The University of Adelaide Press
Print publication year: 2011

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

Save book to Kindle

To save this book to your Kindle, first ensure coreplatform@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×