title: Enhanced apoptosis, oxidative stress and mitochondrial dysfunction in lymphocytes as potential biomarkers for Alzheimer's disease.
abstract: Alzheimer's disease (AD) is the most common progressive neurodegenerative disease. Today, AD affects millions of people worldwide and the number of AD cases will increase with increased life expectancy. The AD brain is marked by severe neurodegeneration like the loss of synapses and neurons, atrophy and depletion of neurotransmitter systems in the hippocampus and cerebral cortex. Recent findings suggest that these pathological changes are causally induced by mitochondrial dysfunction, increased oxidative stress and elevated apoptosis. Until now, AD cannot be diagnosed by a valid clinical method or a biomarker before the disease has progressed so far that dementia is present. Furthermore, no valid method is available to determine which patient with mild cognitive impairment (MCI) will progress to AD. Therefore, a correct diagnosis in the early stage of AD is not only of importance considering that early drug treatment is more effective but also that the psychological burden of the patients and relatives could be decreased. In this review, we discuss the potential role of elevated apoptosis, increased oxidative stress and mitochondrial dysfunction as biomarker for AD in a peripheral cell model, the lymphocytes.
authors.affiliation: Zafes, Biocenter, Department of Pharmacology, University of Frankfurt, Frankfurt, Germany.
authors.forename: K
authors.initials: K
authors.lastname: Leuner
authors.forename: J
authors.initials: J
authors.lastname: Pantel
authors.forename: C
authors.initials: C
authors.lastname: Frey
authors.forename: K
authors.initials: K
authors.lastname: Schindowski
authors.forename: K
authors.initials: K
authors.lastname: Schulz
authors.forename: T
authors.initials: T
authors.lastname: Wegat
authors.forename: K
authors.initials: K
authors.lastname: Maurer
authors.forename: A
authors.initials: A
authors.lastname: Eckert
authors.forename: W E
authors.initials: WE
authors.lastname: Müller
mesh_terms: D000367:Age Factors; D000368:Aged; D000544:Alzheimer Disease / Q000175:diagnosis* / Q000235:genetics / Q000503:physiopathology; D016564:Amyloid beta-Protein Precursor / Q000235:genetics; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D015415:Biomarkers; D001921:Brain / Q000503:physiopathology; D004252:DNA Mutational Analysis; D006801:Humans; D008214:Lymphocytes / Q000502:physiology*; D053078:Membrane Potential, Mitochondrial / Q000502:physiology; D008609:Mental Status Schedule; D028361:Mitochondrial Diseases / Q000175:diagnosis* / Q000503:physiopathology; D009474:Neurons / Q000502:physiology; D009842:Oligopeptides / Q000235:genetics; D018384:Oxidative Stress / Q000502:physiology*; D016716:PC12 Cells; D058255:Protease Nexins; D051381:Rats; D011956:Receptors, Cell Surface / Q000235:genetics; D012307:Risk Factors; D013569:Synapses / Q000502:physiology
chemical_list: D016564:Amyloid beta-Protein Precursor; D015415:Biomarkers; D009842:Oligopeptides; C449186:PS1 antigen; D058255:Protease Nexins; D011956:Receptors, Cell Surface