scholarly journals Nutrients, Microglia Aging, and Brain Aging

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Zhou Wu ◽  
Janchun Yu ◽  
Aiqin Zhu ◽  
Hiroshi Nakanishi
Keyword(s):  
Oxidative Stress ◽  
Cognitive Decline ◽  
Systemic Inflammation ◽  
Brain Aging ◽  
Oxygen Species ◽  
Cellular Activation ◽  
Proinflammatory Mediators ◽  
The World ◽  
Age Dependent ◽  
The Brain

As the life expectancy continues to increase, the cognitive decline associated with Alzheimer’s disease (AD) becomes a big major issue in the world. After cellular activation upon systemic inflammation, microglia, the resident immune cells in the brain, start to release proinflammatory mediators to trigger neuroinflammation. We have found that chronic systemic inflammatory challenges induce differential age-dependent microglial responses, which are in line with the impairment of learning and memory, even in middle-aged animals. We thus raise the concept of “microglia aging.” This concept is based on the fact that microglia are the key contributor to the acceleration of cognitive decline, which is the major sign of brain aging. On the other hand, inflammation induces oxidative stress and DNA damage, which leads to the overproduction of reactive oxygen species by the numerous types of cells, including macrophages and microglia. Oxidative stress-damaged cells successively produce larger amounts of inflammatory mediators to promote microglia aging. Nutrients are necessary for maintaining general health, including the health of brain. The intake of antioxidant nutrients reduces both systemic inflammation and neuroinflammation and thus reduces cognitive decline during aging. We herein review our microglia aging concept and discuss systemic inflammation and microglia aging. We propose that a nutritional approach to controlling microglia aging will open a new window for healthy brain aging.

scholarly journals Oxidative stress in animals: a pathophysiologist's view

2020 ◽  
Vol 2020 (4) ◽  
pp. 10-18
Author(s):  
Dmitriy Gildikov
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Antioxidant System ◽  
Review Article ◽  
Publication Activity ◽  
Pathophysiological Mechanism ◽  
Oxygen Species ◽  
The World ◽  
Intracellular Oxidative Stress

In the review article, from the modern standpoint, oxidative stress is considered as a universal pathophysiological mechanism of the vast majority of diseases in animals. A brief review of the publication activity in the world on this topic; the significance of reactive oxygen species in the physiology and development of intracellular oxidative stress, the role of etiological factors that initiate their hyperproduction are presented, as well the methods of detecting oxidative stress are characterizited. General concepts of the antioxidant system of the animal body are examined, and the pathophysiological targets of oxidative stress in animals are generalized.

Aging

2019 ◽  
pp. 105-112
Author(s):  
Risto Näätänen ◽  
Teija Kujala ◽  
Gregory Light
Keyword(s):  
Hearing Loss ◽  
Speech Perception ◽  
Cognitive Decline ◽  
Temporal Processing ◽  
Brain Aging ◽  
Brain Plasticity ◽  
Part Of Speech ◽  
Memory Traces ◽  
Age Related ◽  
The Brain

This chapter shows that MMN and its magnetoencephalographic (MEG) equivalent MMNm are sensitive indices of aging-related perceptual and cognitive decline. Importantly, the age-related neural changes are associated with a decrease of general brain plasticity, i.e. that of the ability of the brain to form and maintain sensory-memory traces, a necessary basis for veridical perception and appropriate cognitive brain function. MMN/MMNm to change in stimulus duration is particularly affected by aging, suggesting the increased vulnerability of temporal processing to brain aging and accounting, for instance, for a large part of speech-perception difficulties of the aged beyond the age-related peripheral hearing loss.

scholarly journals Aging Brain: Prevention of Oxidative Stress by Vitamin E and Exercise

2009 ◽  
Vol 9 ◽  
pp. 366-372 ◽  
Author(s):  
Sambe Asha Devi
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Cognitive Decline ◽  
Middle Age ◽  
Neuronal Loss ◽  
Aging Brain ◽  
Key Factors ◽  
Esterase Inhibitors ◽  
The Brain ◽  
And Oxidative Stress

With aging, the brain undergoes neuronal loss in many areas. Although the loss of cells in the cerebral cortex, in particular the frontal cortex, has been recognized with aging, the influence of synaptic losses has a larger impact on cognitive decline. Much of the recent research on animals, as well as humans, has been aimed at slowing the cognitive decline through enrichment, and it has been found that the key factors are antioxidants and exercise. Several reports support the concept that regular supplementation of vitamin E and physical activity from as early as middle age can slow the cognitive decline observed during the later years. A few studies have also suggested that exercise is analogous to acetylcholine esterase inhibitors that are also used extensively to treat cognitive impairment and dementia in Alzheimer's disease. In addition, reports also support that vitamin E and exercise may act synergistically to overcome free radical injury and oxidative stress in the aging brain.

scholarly journals Aging and Synaptic Plasticity: A Review

2002 ◽  
Vol 9 (4) ◽  
pp. 217-232 ◽  
Author(s):  
Jorge A. Bergado ◽  
William Almaguer
Keyword(s):  
Neural Plasticity ◽  
Brain Aging ◽  
Long Term Potentiation ◽  
Causal Link ◽  
Term Potentiation ◽  
Gradual Loss ◽  
Age Dependent ◽  
Affective Influences ◽  
The Brain

Aging affects all systems, but the brain seems to be particularly vulnerable to the action of negative, age-dependent factors. A gradual loss of memory functions is one of the earliest and most widespread consequences of brain aging. The causes for such impairment are still unclear. Long-term potentiation (LTP) is one form of neural plasticity, which has been proposed as the cellular correlate for memory. LTP is affected by aging, and such alteration might be causally related to memory dysfunction. In the present paper, we review the evidence sustaining the existence of a causal link between cognitive and LTP impairments, as well as the possible mechanisms involved. New results indicate a possible involvement of a deficient reinforcement of LTP by affective influences.

MPTP-induced oxidative stress and neurotoxicity are age-dependent: Evidence from measures of reactive oxygen species and striatal dopamine levels

Synapse ◽  
1994 ◽  
Vol 18 (1) ◽  
pp. 27-34 ◽  
Author(s):  
Syed F. Ali ◽  
Stanley N. David ◽  
Glenn D. Newport ◽  
Jean L. Cadet ◽  
William Slikker
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Striatal Dopamine ◽  
Oxygen Species ◽  
Age Dependent

Neuroprotective effect of Decalepis hamiltonii on cyclophosphamide-induced oxidative stress in the mouse brain

2016 ◽  
Vol 0 (0) ◽  
Author(s):  
Mahsa Zarei ◽  
T. Shivanandappa
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Side Effects ◽  
Mouse Brain ◽  
Neuroprotective Effect ◽  
Oxygen Species ◽  
Glutathione S Transferase ◽  
Decalepis Hamiltonii ◽  
Expression Of Genes ◽  
The Brain

AbstractCyclophosphamide (CP), one of the most widely used antineoplastic drugs, causes toxic side effects on vital organs including brain. In this study, we have investigated neuroprotective potential of the aqueous extract of the roots ofSwiss albino male mice were pre-treated with DHA (50 and 100 mg/kg b.w.) for 10 consecutive days followed by an injection with CP intraperitoneally (25 mg/kg b.w.) for 10 days 1 h after DHA treatment; 16 h later, they were euthanized, their brains were immediately removed, and biochemical and molecular analyses were conducted.The results indicated that injection of CP induced oxidative stress in the mouse brain as evident from the increased lipid peroxidation, reactive oxygen species, depletion of glutathione and reduced activities of the antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione-S-transferase. Treatment with DHA significantly mitigated the CP-induced oxidative stress. Moreover, expression of genes for the antioxidant enzymes was downregulated by CP treatment which was reversed by DHA.In conclusion, DHA protected the brain from oxidative stress induced by CP, and therefore, it could be a promising nutraceutical as a supplement in cancer chemotherapy in order to ameliorate the toxic side effects of cancer drugs.

scholarly journals Antioxidant and Astroprotective Effects of aPulicaria incisaInfusion

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Anat Elmann ◽  
Alona Telerman ◽  
Sharon Mordechay ◽  
Hilla Erlank ◽  
Rivka Ofir
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Brain Injuries ◽  
Desert Plant ◽  
Oxygen Species ◽  
Intracellular Accumulation ◽  
Glial Derived Neurotrophic Factor ◽  
The Brain ◽  
Antioxidant Effects

Oxidative stress is involved in the pathogenesis of neurodegenerative diseases such as Parkinson's and Alzheimer's diseases. Astrocytes, the most abundant glial cells in the brain, protect neurons from reactive oxygen species (ROS) and provide them with trophic support, such as glial-derived neurotrophic factor (GDNF). Thus, any damage to astrocytes will affect neuronal survival. In the present study, an infusion prepared from the desert plantPulicaria incisa(Pi) was tested for its protective and antioxidant effects on astrocytes subjected to oxidative stress. ThePiinfusion attenuated the intracellular accumulation of ROS following treatment with hydrogen peroxide and zinc and prevented the H2O2-induced death of astrocytes. ThePiinfusion also exhibited an antioxidant effectin vitroand induced GDNF transcription in astrocytes. It is proposed that thisPiinfusion be further evaluated for use as a functional beverage for the prevention and/or treatment of brain injuries and neurodegenerative diseases in which oxidative stress plays a role.

scholarly journals Increased Tyrosine Nitration of the Brain in Chronic Renal Insufficiency: Reversal by Antioxidant Therapy and Angiotensin-Converting Enzyme Inhibition

2001 ◽  
Vol 12 (9) ◽  
pp. 1892-1899
Author(s):  
GANGMIN DENG ◽  
NOSRATOLA D. VAZIRI ◽  
BAHMAN JABBARI ◽  
ZHEMIN NI ◽  
XIAO-XIN YAN
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Cerebral Cortex ◽  
Antioxidant Therapy ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Tyrosine Nitration ◽  
Oxygen Species ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibition ◽  
The Brain

Abstract. Interaction of reactive oxygen species with nitric oxide promotes nitric oxide inactivation and generation of cytotoxic reactive nitrogen species that attack DNA, lipids, and proteins. Nitration of free tyrosine and tyrosine residues of proteins results in production of nitrotyrosine, which can lead to excitotoxicity and frequently is found in the brain of patients and animals with various degenerative, ischemic, toxic, and other neurologic disorders. According to earlier studies, reactive oxygen species activity is increased and neuronal NO synthase expression in the brain is elevated in animals with chronic renal failure (CRF). It was hypothesized, therefore, that tyrosine nitration must be increased in the uremic brain. This hypothesis was tested, through determination of nitrotyrosine abundance (by Western blot analysis), as well as distribution (by immunohistology), in the cerebrum of rats with CRF 6 wk after 5/6 nephrectomy. The results were compared with those of sham-operated controls and antioxidant (lazaroid)-treated and captopril-treated rats with CRF. Western blot analysis revealed a significant increase in nitrotyrosine abundance in the cerebral cortex of rats with CRF. This was accompanied by an intense nitrotyrosine staining of the neuronal processes, including proximal segments of dendrites, axons, and axon terminals of the cortical neurons. Both antioxidant therapy and captopril administration alleviated oxidative stress (as evidenced by normalization of plasma lipid peroxidation product malondialdehyde) and significantly reduced nitrotyrosine abundance in the cerebral cortex of the treated CRF group. In conclusion, CRF resulted in oxidative stress and increased tyrosine nitration in the cerebral cortex. Antioxidant therapy and angiotensin-converting enzyme inhibition alleviated the CRF-induced oxidative stress and mitigated tyrosine nitration in the rats with CRF.

scholarly journals Responses of Plants to Pesticide Toxicity: an Overview

2019 ◽  
Vol 37 ◽  
Author(s):  
A. SHARMA ◽  
V. KUMAR ◽  
A.K. THUKRAL ◽  
R. BHARDWAJ
Keyword(s):  
Oxidative Stress ◽  
Photosynthetic Efficiency ◽  
Physiological Responses ◽  
Enzymatic Antioxidants ◽  
Oxygen Species ◽  
Defense System ◽  
Negative Effects ◽  
Pesticide Toxicity ◽  
Pesticide Stress ◽  
The World

ABSTRACT: Pesticides are applied all over the world to protect plants from pests. However, their application also causes toxicity to plants, which negatively affects the growth and development of plants. Pesticide toxicity results in reduction of chlorophyll and protein contents, accompanied by decreased photosynthetic efficiency of plants. Pesticide stress also generates reactive oxygen species which causes oxidative stress to plants. To attenuate the negative effects of oxidative stress, the antioxidative defense system of plants gets activated, and it includes enzymatic antioxidants as well as non-enzymatic antioxidants. The present review gives an overview of various physiological responses of plants under pesticide toxicity in tabulated form.

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