Fariba Khodagholi, Fatemeh Shaerzadeh* and Fateme Montazeri Pages 973 - 985 ( 13 )
Background: Mitochondrial aconitase (Aco2), a member of the family of iron-sulfur [4Fe- 4S]-containing dehydratases, is involved in cellular metabolism through the tricarboxylic acid cycle. Aco2 is highly susceptible to oxidative damage in a way that exposure to the reactive species and free radicals leads to release of iron from the central [4Fe-4S] cluster resulting in the production of the inactive form of Aco2.
Objective: There is increasing evidence supporting a direct association between impaired energy metabolism and the incidence and progression of neurodegenerative disorders in neuronal cells.
Results: It has been shown that alteration in bioenergetic parameters is a common pathological feature of the neurodegenerative diseases leading to neuronal dysfunction. Numerous studies have demonstrated that dysfunctional Aco2, among the other bioenergetic parameters, is a key factor that could promote neurodegeneration.
Conclusion: Increasing our knowledge about energy metabolism-related molecules including Aco2 affected by neurodegenerative disorders might be useful to find an efficient therapeutic strategy for those central nervous system-related diseases. Accordingly, in this review, we have focused on the events and processes that occur in neurodegeneration, leading to the inactivation of Aco2 in the brain.
Mitochondrial aconitase, neurodegenerative disorders, oxidative stress, iron-sulfur cluster, Alzheimer's disease.
Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Molecular Medicine Research Center, Hormozgan Health Institute, Hormozgan University of Medical Sciences, Bandar Abbas, NeuroBiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran