Caffeine prevents d-galactose-induced cognitive deficits, oxidative stress, neuroinflammation and neurodegeneration in the adult rat brain

Fett

et al. 2016

AJTCAM

Background: Intense physical training increases oxidative stress and inflammation, resulting into muscle and cellular damage. The aim of this study was to analyze the effect of caffeine supplementation on trained young individuals subjected to two treadmill maximal tests. Materials and Methods: It was a double-blind and crossover study comprising 24 active individuals within the age group 18-30 years. The comparisons were conducted: the effect of exercise (week 1 x 2) and caffeine intake (GC x GP) on thiobarbituric acid (TBARS), interleukin 6 (IL-6), interleukin 10 (IL-10) and superoxide dismutase (SOD) variables during pre-exercise time (30 min. after caffeine or placebo intake) and post-exercise (5 min after treadmill test). Results:The comparison between weeks 1 and 2 showed increase in the first week, in the following items: TBARS, IL-6 and IL-10 in the GC and GP groups. The comparison within the same week showed that GC individuals presented lower post-exercise TBARS values in the first and second weeks; IL-6 presented higher post-exercise values in the GC group in both weeks. The paired analysis comparing pre-and post-exercise, with and without caffeine showed that IL-6 presented higher post-exercise values in the GC group. Conclusion: Caffeine used by athletes can decrease oxidative stress. The increased IL-6 suggest that this ergogenic supplement may stimulate muscle hypertrophy, since IL-6 has myokine effect. However, the caffeine effect on IL-6 level and muscle hypertrophy increase should be better investigated in future studies.

Section: Discussionmentioning

confidence: 89%

The Effect of Caffeine Supplementation on Trained Individuals Subjected to Maximal Treadmill Test

Fett

et al. 2016

AJTCAM

“…In fact, chronic caffeine intake ameliorates oxidative stress and improves mitochondrial function in several neurotoxic situations . A study in rats showed that caffeine reversed oxidative stress and attenuated inflammation induced by d ‐galactose, a compound that can induce aging in rat brains . As well, caffeine increases glutathione S‐transferase activity and inhibits red blood cell membrane derangement and apoptosis .…”

Section: Caffeinementioning

confidence: 99%

The neuroprotective effects of caffeine in neurodegenerative diseases

2017

Caffeine is the most widely used psychostimulant in Western countries, with antioxidant, anti-inflammatory and anti-apoptotic properties. In Alzheimer's disease (AD), caffeine is beneficial in both men and women, in humans and animals. Similar effects of caffeine were observed in men with Parkinson's disease (PD); however, the effect of caffeine in female PD patients is controversial due to caffeine's competition with estrogen for the estrogen-metabolizing enzyme, CYP1A2. Studies conducted in animal models of amyotrophic lateral sclerosis (ALS) showed protective effects of A R antagonism. A study found caffeine to be associated with earlier age of onset of Huntington's disease (HD) at intakes >190 mg/d, but studies in animal models have found equivocal results. Caffeine is protective in AD and PD at dosages equivalent to 3-5 mg/kg. However, further research is needed to investigate the effects of caffeine on PD in women. As well, the effects of caffeine in ALS, HD and Machado-Joseph disease need to be further investigated. Caffeine's most salient mechanisms of action relevant to neurodegenerative diseases need to be further explored.

Drug Development Research

“…High ratios of BAX:BCL2 promote the activation of caspases and induce apoptosis [Ullah et al, 2015]. Studies that have examined markers of apoptosis and levels of apoptotic regulatory proteins such as BAX in postmortem AD and PD brain tissues found the ratios of BAX:BCL2 higher than normal [Fern andezMoriano et al, 2015;Tripathy et al, 2015].…”

Section: Apoptotic Priming In Mitochondriamentioning

confidence: 99%

Epigenetic Treatment of Neurodegenerative Disorders: Alzheimer and Parkinson Diseases

Irwin

Moos

Faller

et al. 2016

Preclinical Research In this review, we discuss epigenetic-driven methods for treating neurodegenerative disorders associated with mitochondrial dysfunction, focusing on carnitinoid antioxidant-histone deacetylase inhibitors that show an ability to reinvigorate synaptic plasticity and protect against neuromotor decline in vivo. Aging remains a major risk factor in patients who progress to dementia, a clinical syndrome typified by decreased mental capacity, including impairments in memory, language skills, and executive function. Energy metabolism and mitochondrial dysfunction are viewed as determinants in the aging process that may afford therapeutic targets for a host of disease conditions, the brain being primary in such thinking. Mitochondrial dysfunction is a core feature in the pathophysiology of both Alzheimer and Parkinson diseases and rare mitochondrial diseases. The potential of new therapies in this area extends to glaucoma and other ophthalmic disorders, migraine, Creutzfeldt-Jakob disease, post-traumatic stress disorder, systemic exertion intolerance disease, and chemotherapy-induced cognitive impairment. An emerging and hopefully more promising approach to addressing these hard-to-treat diseases leverages their sensitivity to activation of master regulators of antioxidant and cytoprotective genes, antioxidant response elements, and mitophagy. Drug Dev Res 77 : 109-123, 2016. © 2016 Wiley Periodicals, Inc.