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Front Neurosci. 2018 Aug 13;12:533. doi: 10.3389/fnins.2018.00533. eCollection 2018.

Dysregulation of Neuronal Iron Homeostasis as an Alternative Unifying Effect of Mutations Causing Familial Alzheimer's Disease.

Frontiers in neuroscience

Amanda L Lumsden, Jack T Rogers, Shohreh Majd, Morgan Newman, Greg T Sutherland, Giuseppe Verdile, Michael Lardelli

Affiliations

  1. College of Medicine and Public Health, Flinders University, Adelaide, SA, Australia.
  2. South Australian Health and Medical Research Institute, Adelaide, SA, Australia.
  3. Neurochemistry Laboratory, Department of Psychiatry-Neuroscience, Massachusetts General Hospital (East), Harvard Medical School, Harvard University, Charlestown, MA, United States.
  4. Neuronal Injury and Repair Laboratory, Centre for Neuroscience, College of Medicine and Public Health, Flinders University, Adelaide, SA, Australia.
  5. Centre for Molecular Pathology, School of Biological Sciences, University of Adelaide, Adelaide, SA, Australia.
  6. Discipline of Pathology, Sydney Medical School, University of Sydney, Sydney, NSW, Australia.
  7. School of Pharmacy and Biomedical Sciences, Faculty of Health Sciences, Curtin Health Innovation Research Institute, Curtin University, Bentley, WA, Australia.

PMID: 30150923 PMCID: PMC6099262 DOI: 10.3389/fnins.2018.00533

Abstract

The overwhelming majority of dominant mutations causing early onset familial Alzheimer's disease (EOfAD) occur in only three genes,

Keywords: AMYLOID BETA A4 PRESCURSOR PROTEIN; PRESENILIN; familial Alzheimer’s disease; iron homeostasis; mutation; neurodegeneration; secretase; trafficking

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