Role of D-galactose-induced brain aging and its potential used for therapeutic interventions
Authors: Wasana Pratchayasakul
Thazin Shwe
Nipon Chattipakorn
Siriporn C Chattipakorn
Journal: Experimental gerontology (2018)
Discipline: CLINICAL MEDICINE
Keywords: Brain aging; Cognitive function; D-galactose; Mitochondria; Therapeutic.
Affiliations: Neurophysiology unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Center of Excellence in Cardiac Electrophysiology, Chiang Mai University, Chiang Mai 50200, Thailand., Neurophysiology unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand; Center of Excellence in Cardiac Electrophysiology, Chiang Mai University, Chiang Mai 50200, Thailand; Department of Oral Biology and Diagnostic Sciences, Faculty of Dentistry, Chiang Mai University, Chiang Mai, 50200, Thailand. Electronic address: .

Abstract:  Aging is a phenomenon that all living organisms inevitably face. Every year, 9.9million people, globally, suffer from dementia, an indicator of the aging brain. Brain aging is significantly associated with mitochondrial dysfunction. This is characterized by a decrease in the activity of respiratory chain enzymes and ATP production, and increased free radical generation, mitochondrial deoxyribonucleic acid (DNA) mutations, and impaired mitochondrial structures. To get a better understanding of aging and to prevent its effects on many organs, chronic systemic administration of D-galactose was used to artificially create brain senescence in animal models and established to be beneficial for studies of anti-aging therapeutic interventions. Several studies have shown that D-galactose-induced brain aging which does so not only by causing mitochondrial dysfunction, but also by increasing oxidative stress, inflammation, and apoptosis, as well as lowering brain-derived neurotrophic factors. All of these defects finally lead to cognitive decline. Various therapeutic approaches which act on mitochondria and cognition were evaluated to assess their effectiveness in the battle to reverse brain aging. The aim of this article is to comprehensively summarize and discuss the underlying mechanisms involved in D-galactose-induced brain aging, particularly as regards alterations in brain mitochondria and cognitive function. In addition, the aim is to summarize the different therapeutic approaches which have been utilized to address D-galactose-induced brain aging. 

Retracted: No

PubPeer comments:
 Galactose oxidase-mediated generation of H2O2 has been referred to as an important pathophysiological mechanism in the context of D-galactose-induced brain aging in rodents throughout the text and in Fig.1. However, galactose oxidase is a fungal enzyme so it is hard to understand how it can mediate detrimental effects in rodents? A comment on the topic entitled:  Separating science from science fiction: A non-existent enzyme is a primary driver of pathophysiological processes in galactose-induced rodent models of aging is available here: https: bit.ly 2ZVJMh9 ,