Affiliations: [a] Department of Psychiatry and Psychotherapy, RWTH Aachen University, Aachen, Germany | [b] Clinical Neurochemistry, University Clinic & Policlinic Psychiatry, Psychosomatic and Psychotherapy, University of Würzburg, Würzburg, Germany | [c] JARA – Translational Brain Medicine, Aachen, Germany | [d] State Hospital for Psychiatry, Psychotherapy and Neurology, Lohr am Main, Germany | [e] Department of Neuropathology, Institute of Pathology, University of Würzburg, Germany
Correspondence:
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Correspondence to: Tanja Maria Michel, MD, Department of Psychiatry and Psychotherapy, RWTH Aachen University, Pauwelsstraße 30, 52074 Aachen, Germany. Tel.: +49 2418036258; Fax: +49 2418082524; E-mail: tmichel@ukaachen.
Abstract: For decades, it has been acknowledged that oxidative stress due to free radical species contributes to the pathophysiology of aging and neurodegenerative diseases. Aldehyde dehydrogenases (ALDH) not only transform aldehydes to acids but also act as antioxidant enzymes. However, little is known about the implications of the enzymatic family of ALDH in the context of neurodegenerative processes such as Alzheimer's disease (AD). We therefore examined the enzymatic activity of the mitochondrial ALDH-isoform in different regions of the postmortem brain tissue isolated from patients with AD and controls. We found that the mitochondrial ALDH activity was significantly increased only in the putamen of patients suffering from AD compared to controls. This is of particular interest since mediators of oxidative stress, such as iron, are increased in the putamen of patients with AD. This study adds to the body of evidence that suggests that oxidative stress as well as aldehyde toxicity play a role in AD.
