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Journal of Alzheimer’s Disease 44 (2015) 649–660 DOI 10.3233/JAD-142052 IOS Press
Lymphocytic Mitochondrial Aconitase Activity is Reduced in Alzheimer’s Disease and Mild Cognitive Impairment Francesca Mangialaschea,b , Mauro Baglionia , Roberta Cecchettia , Miia Kivipeltob , Carmelinda Ruggieroa , Danilo Piobbicoc , Lothar Kussmauld , Roberto Monasteroe , Stefano Brancorsinic,∗ and Patrizia Mecoccia,∗ a Section
of Gerontology and Geriatrics, Department of Medicine, University of Perugia, Perugia, Italy Research Center, Karolinska Institutet-Stockholm University, Stockholm, Sweden c Department of Experimental Medicine - Section of Terni, University of Perugia, Italy d Department of Central Nervous System Research, Boehringer-Ingelheim Pharma GmbH & Co, Biberach an der Riss, Germany e Section of Neurology, Department of Experimental Biomedicine and Clinical Neuroscience, University of Palermo, Palermo, Italy b Aging
Handling Associate Editor: Domenico Pratico Accepted 16 September 2014
Abstract. Background: Specific mechanisms behind the role of oxidative/nitrosative stress and mitochondrial dysfunction in Alzheimer’s disease (AD) pathogenesis remain elusive. Mitochondrial aconitase (ACO2) is a Krebs cycle enzyme sensitive to free radicalmediated damage. Objective: We assessed activity and expression of ACO2 extracted from blood lymphocytes of subjects with AD, mild cognitive impairment (MCI), older adults with normal cognition (OCN, age ≥65 years), and younger adults with normal cognition (YCN, age
Journal of Alzheimer’s Disease 44 (2015) 649–660 DOI 10.3233/JAD-142052 IOS Press
Lymphocytic Mitochondrial Aconitase Activity is Reduced in Alzheimer’s Disease and Mild Cognitive Impairment Francesca Mangialaschea,b , Mauro Baglionia , Roberta Cecchettia , Miia Kivipeltob , Carmelinda Ruggieroa , Danilo Piobbicoc , Lothar Kussmauld , Roberto Monasteroe , Stefano Brancorsinic,∗ and Patrizia Mecoccia,∗ a Section
of Gerontology and Geriatrics, Department of Medicine, University of Perugia, Perugia, Italy Research Center, Karolinska Institutet-Stockholm University, Stockholm, Sweden c Department of Experimental Medicine - Section of Terni, University of Perugia, Italy d Department of Central Nervous System Research, Boehringer-Ingelheim Pharma GmbH & Co, Biberach an der Riss, Germany e Section of Neurology, Department of Experimental Biomedicine and Clinical Neuroscience, University of Palermo, Palermo, Italy b Aging
Handling Associate Editor: Domenico Pratico Accepted 16 September 2014
Abstract. Background: Specific mechanisms behind the role of oxidative/nitrosative stress and mitochondrial dysfunction in Alzheimer’s disease (AD) pathogenesis remain elusive. Mitochondrial aconitase (ACO2) is a Krebs cycle enzyme sensitive to free radicalmediated damage. Objective: We assessed activity and expression of ACO2 extracted from blood lymphocytes of subjects with AD, mild cognitive impairment (MCI), older adults with normal cognition (OCN, age ≥65 years), and younger adults with normal cognition (YCN, age
