Copper Status in Alzheimer's Disease and other Neurodegenerative Disorders: Genetics, Mechanisms, Neurophysiology, and Therapies
1Department of Neuroscience, AFaR, Ospedale Fatebenefratelli, Isola Tiberina, Rome, Italy
2Department of Neurology, University Hospital Utrecht, Utrecht, The Netherlands
3Roberts Laboratory for Neurodegenerative Disease Research, Sun Health Research Institute, Sun City, AZ, USA
4Departments of Human Genetics and Internal Medicine, University of Michigan Medical School, 5022 Kresge Building II, Ann Arbor, MI, USA
Copper Status in Alzheimer's Disease and other Neurodegenerative Disorders: Genetics, Mechanisms, Neurophysiology, and Therapies
Description
Alzheimer's disease (AD) is a leading cause of death worldwide. It is a genetically heterogeneous syndrome which includes a broad spectrum of phenotypes. Recent advances in biology and medicine have introduced metals, particularly copper, as influencing agents in AD, thus improving understanding of the mechanisms and electrophysiology underlying the pathology. Increasing information has led to the development of new models or tools to characterize defective pathways of copper trafficking linked to neurodegenerative processes and the rational for phase II and III clinical trials as well.
We invite investigators to contribute original research articles as well as review articles that will stimulate the continuing efforts to understand the molecular pathology underlying copper involvement in AD. Potential topics include, but are not limited to:
- Advances in metal toxicity as well as genetics of AD
- Latest technologies or strategies to point out metallobiological processes subtending typical deficits of AD
- Role of inflammation related to copper status in AD
- Metal-proteins interplay in AD, in mild cognitive impairment, and in other copper diseases of neurodegeneration other than AD
- Recent advances in drug strategy based on metallobiology of AD as well as biological molecules which induce or maintain a state of copper malabsorption
- The increased toxicity of oral ingestion of inorganic copper (such as in drinking water or copper supplements) relative to organically bound copper in food
- The interaction of lipids, for example, from a high fat diet, and copper in producing neurotoxicity
- The mechanisms whereby aging increases susceptibility to copper toxicity in the brain
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