INTRODUCTION:

Many elderly individuals live with memory problems that are part of the normal aging process. Cognitive deficits, such as learning impairment and delayed amnesia, are striking, debilitating consequences of normal and pathological aging in humans. Multiple mechanisms are implicated in the development of age-associated memory impairment including age-related alterations in the central nervous system that may contribute to neuronal cell damage due to increased formation of reactive oxygen species (ROS) and a deteriorated antioxidant defense system [1, 2]. As the average life span continues to lengthen, it is critical to minimize the development of cognitive defects in elderly people.

Recent evidence suggests that molecular hydrogen potently protects the central nervous system by eliminating ROS [3]. Likewise, drinking hydrogen water (HW) prevented chronic physical restraint-induced impairments of learning tasks [4, 5]. More recently, hydrogen in drinking water reduced dopaminergic neuronal loss in a mouse model of Parkinson's disease induced by administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine [6]. Based on these observations, we hypothesized that oral intake of hydrogen via HW may reduce oxidative stress in the aging brain and ameliorate cognitive loss in aged mice.

In the present study, we have used a senescence-accelerated mouse (SAM) model, which is a well-accepted animal model of age-related cognitive impairment, to examine the influence of HW on brain activity and memory loss. SAMs were developed by selectively breeding AKR/J mice and are classified as senescence-prone or senescence-resistant based on senescence (as assessed by a scoring system) pathological phenotype, and lifespan [7, 8]. Senescence-accelerated prone mouse 8 (SAMP8) is an appropriate model of aging-associated senescence and has impairments in nonspatial learning and memory beginning as early as 2 months of age. The SAMP8 mice have a higher oxidative stress status that is partly caused by mitochondrial dysfunction and results in the excessive production of ROS and neurodegeneration [9]. Although protective effects of hydrogen have been postulated in several degenerative neuronal disease models, this study is the first report demonstrating the efficacies of hydrogen in a senescence-related cognitive disorder. Our method of HW production with a portable magnesium stick is safe, cost-effective and ideal for elderly people, as it can be administered without changing their lifestyle. Drinking HW daily may be a promising preventative approach for age-related neurodegenerative disease and have an enormous impact on future healthcare for the elderly.

ABSTRACT:

Hydrogen has been reported to have neuron protective effects due to its antioxidant properties, but the effects of hydrogen on cognitive impairment due to senescence-related brain alterations and the underlying mechanisms have not been characterized. In this study, we investigated the efficacies of drinking hydrogen water for prevention of spatial memory decline and age-related brain alterations using senescence-accelerated prone mouse 8 (SAMP8), which exhibits early aging syndromes including declining learning ability and memory. However, treatment with hydrogen water for 30 days prevented age-related declines in cognitive ability seen in SAMP8 as assessed by a water maze test and was associated with increased brain serotonin levels and elevated serum antioxidant activity. In addition, drinking hydrogen water for 18 weeks inhibited neurodegeneration in hippocampus, while marked loss of neurons was noted in control, aged brains of mice receiving regular water. On the basis of our results, hydrogen water merits further investigation for possible therapeutic/preventative use for age-related cognitive disorders.

Keywords: hydrogen water, magnesium stick, senescence, oxidative stress, cognitive disorder

STUDY NAME:

Drinking Hydrogen Water Ameliorated Cognitive Impairment in Senescence-Accelerated Mice

Yeunhwa Gu,¹ Chien-Sheng Huang,^2,3 Tota Inoue,¹ Takenori Yamashita,¹ Torao Ishida,¹ Ki-Mun Kang,⁴ and Atsunori Nakao,^3
1Graduate School of Health Science, Suzuka University of Medical Science, Suzuka, Mie 510-0293, Japan
²Division of Thoracic Surgery, Department of Surgery, Taipei-Veterans General Hospital and National Yang-Ming University, School of Medicine, Taipei 112 Taiwan
³Department of Surgery, University of Pittsburgh Medical Center, E1551 Biomedical Science Tower, 200 Lothrop Street, Pittsburgh, PA 15213, USA
⁴Department of Therapeutic Radiology, Gyeongsang National University Hospital, Gyeongsang Institute of Health Sciences, 900 Gaiwa-dong, Jinju 660-701, Korea

FOR FURTHER READING VISIT FOLLOWING LINK:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872234/