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BioMed Research International
Volume 2014, Article ID 648740, 8 pages
Review Article

Shared Mechanisms of Neurodegeneration in Alzheimer’s Disease and Parkinson’s Disease

1Department of Neurology, Affiliated Hospital of Medical College, Qingdao University, Qingdao, Shandong 266003, China
2Department of Endocrinology, Affiliated Hospital of Medical College, Qingdao University, No. 16 Jiangsu Road, Qingdao, Shandong 266003, China

Received 8 February 2014; Revised 16 April 2014; Accepted 20 April 2014; Published 12 May 2014

Academic Editor: Jin-Tai Yu

Copyright © 2014 Anmu Xie et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Alzheimer’s disease (AD) and Parkinson’s disease (PD) have markedly different clinical and pathological features, but these two diseases are the most common neurodegenerative disorders. Previous studies have showed that there are common mechanisms in AD and PD. Several genetic studies have revealed mutations in genes associated with the risk of AD and PD. Circumstantial evidences have shown that dysregulation of brain iron homeostasis leads to abnormal iron accumulation and results in AD as well as PD. α-Synuclein and tau take part in the mechanisms of these diseases by oxidative stress and mitochondrial dysfunction. Some studies indicated that the loss of LC noradrenergic neurons may occur early in the progression of AD and PD. Nicotinic acetylcholine receptors (nAChRs) are members of the Cys-loop superfamily of pentameric ligand-gated ion channels; some evidence showed that nicotinic receptors may be associated with AD and PD. These experimental and clinical studies may provide a scientific foundation for common shared mechanisms in AD and PD.