Osteoporosis disease is a metabolic disorder in which bone mineral density (BMD) is lower than the normal threshold. Based on literature, it is known that schizophrenic patients due to consuming anti-psychotic drugs and Parkinson’s disease patients due to vitamin D deficiency and decrease in mobility are at the high risk of osteoporosis (1–4).
On the other hand, it is observed that adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) activity, which is regulating cellular energy homeostasis, is reduced in schizophrenia diseases (5). In addition, it is known that there is mitochondrial dysfunction in Parkinson’s disease that can be treated by AMPK, which is identified as a mitochondrial biogenesis (6–8). Recently, some findings show that AMPK plays an important role in bone metabolism. Besides, some in vitro studies revealing that AMPK modulators regulate bone cell function (9–13). Also, some studies show that deficiency of AMPK α and β subunits in mice causes bone loss in vivo (14).
Based on the above mentioned points, it can be referred that AMPK deficiency in Parkinson’s disease and schizophrenia may lead to osteoporosis. This can be used as a goal in treatment of osteoporosis in those disorders. In another word, nowadays there are some drugs available for both diseases but they have some side effect, which may lead to osteoporosis; by considering the fact that AMPK deficiency may cause osteoporosis, new drugs can be provided with AMPK supplement to reduce the osteoporosis symptoms. Surely, experimental trials are needed to validate our hypothesis.
Statements
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
References
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Summary
Keywords
Parkinson’s disease, schizophrenia, osteoporosis, AMPK, energy metabolism
Citation
Radaei F, Darvishi A and Gharibzadeh S (2014) The Correlation between Osteoporosis Occurrences in Both Schizophrenia and Parkinson’s Disease. Front. Neurol. 5:83. doi: 10.3389/fneur.2014.00083
Received
13 February 2014
Accepted
16 May 2014
Published
02 June 2014
Volume
5 - 2014
Edited by
Jordi Blanch, Hospital Clínic de Barcelona, Spain
Reviewed by
Varun Kesherwani, University of Nebraska Medical Center, USA
Copyright
© 2014 Radaei, Darvishi and Gharibzadeh.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: gharibzadeh@aut.ac.ir
This article was submitted to Neurodegeneration, a section of the journal Frontiers in Neurology.
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