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Journal of Biomedicine and Biotechnology
Volume 2006, Article ID 24038, 5 pages
Research Article

Heme Deficiency in Alzheimer’s Disease: A Possible Connection to Porphyria

1Research Service (151), VA Medical ’ Regional Office Center, White River Junction, VT 05009, USA
2Department of Medicine (Neurology), Dartmouth Medical School, Hanover, NH 03755, USA
3Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA

Received 1 December 2005; Revised 30 March 2006; Accepted 5 April 2006

Copyright © 2006 Barney E. Dwyer 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.


Mechanisms that cause Alzheimer’s disease (AD), an invariably fatal neurodegenerative disease, are unknown. Important recent data indicate that neuronal heme deficiency may contribute to AD pathogenesis. If true, factors that contribute to the intracellular heme deficiency could potentially alter the course of AD. The porphyrias are metabolic disorders characterized by enzyme deficiencies in the heme biosynthetic pathway. We hypothesize that AD may differ significantly in individuals possessing the genetic trait for an acute hepatic porphyria. We elaborate on this hypothesis and briefly review the characteristics of the acute hepatic porphyrias that may be relevant to AD. We note the proximity of genes encoding enzymes of the heme biosynthesis pathway to genetic loci linked to sporadic, late-onset AD. In addition, we suggest that identification of individuals carrying the genetic trait for acute porphyria may provide a unique resource for investigating AD pathogenesis and inform treatment and management decisions.