ROS and Brain Diseases: The Good, the Bad, and the Ugly

Popa‐Wagner, Aurel; Mitran, Smaranda Ioana; Sivanesan, Senthilkumar; Chang, Edwin; Buga, Ana-Maria

doi:10.1155/2013/963520

Cited by 338 publications

(242 citation statements)

References 173 publications

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“…Previous reports have demonstrated that, under normal conditions, supplementation of CoQ10 [36, 37] or other antioxidant agents does not improve memory performance [9]. Elevated levels of reactive oxygen species are involved in numerous diseases, and they play a key role in several normal physiological processes and signaling pathways of cognitive processes [38-41]. Thus, increasing antioxidant levels and activities in physiological conditions have no beneficial effects on cognition and may even contribute to a decline in this process.…”

Section: Discussionmentioning

confidence: 99%

Influence of Chronic Coenzyme Q10 Supplementation on Cognitive Function, Learning, and Memory in Healthy and Diabetic Middle-Aged Rats

2018

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Diabetes mellitus can induce impairment in learning and memory. Cognitive and memory deficits are common in older adults and especially in those with diabetes. This is mainly because of hyperglycemia, oxidative stress, and vascular abnormalities. Coenzyme Q10 (CoQ10) can decrease oxidative stress, hyperglycemia, and inflammatory markers, and improve vascular function. Therefore, the aim of the present study was to investigate the possible effects of CoQ10 on cognitive function, learning, and memory in middle-aged healthy and diabetic rats. Adult middle-aged male Wistar rats (390–460 g, 12–13 months old) were divided into 6 experimental groups. Diabetes was induced by a single i.p. injection of streptozotocin (60 mg/kg). CoQ10 (20 or 120 mg/kg, orally by gavage) was administered for 45 days. The cognitive function and learning memory of rats were evaluated using novel object recognition (NOR) and passive avoidance tests. The discrimination index of the NOR test in the diabetic groups receiving CoQ10 (20 or 120 mg/kg) and the healthy group receiving CoQ10 (120 mg/kg) was significantly higher than that in the control group. In addition, the step through latency was significantly longer and the time spent in the dark compartment was significantly shorter in the diabetic groups receiving CoQ10 than in the control group. CoQ10 supplementation can improve learning and memory deficits induced by diabetes in older subjects. In addition, CoQ10 at higher doses can improve cognitive performance in older healthy subjects.

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Section: Discussionmentioning

confidence: 99%

Influence of Chronic Coenzyme Q10 Supplementation on Cognitive Function, Learning, and Memory in Healthy and Diabetic Middle-Aged Rats

2018

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“…An increase in the level of reactive oxygen species (oxygen ions, free radicals and peroxides) leads to oxidative stress, which would alter the neuronal signals that produce neuro-inlammation with neuro-degeneration and implicitly with cognitive impairment [67].…”

Section: Copd: Fundamental Pathophysiological Mechanisms Susceptible mentioning

confidence: 99%

Neurocognitive Impairment as Systemic Effects of COPD

Oancea¹,

Tudorache²,

Tudorache³

2018

COPD - An Update in Pathogenesis and Clinical Management

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Mild cognitive impairment (MCI), also known as incipient dementia, is characterized by the decline of cognitive function greater than expected for a certain age and educational level of the individual but not severe enough to interfere with their daily activities. However, this mild cognitive impairment afects several areas: visuospatial, memory, atention and luency and it is a signiicant concern because it decreases the quality of life and treatment adherence of these patients. On the other hand, evidence suggests that individuals with Chronic obstructive pulmonary disease (COPD) also present an important risk of falls: 46% of these patients experience a fall/year, sometimes with fatal consequences. Standard clinical balance measures can predict the risk of falls in this population. Moreover, increased inlammatory biomarkers are associated with the decrease of cognitive functions and a higher risk of falls in this population. Patients with COPD have a higher balance and cognitive impairment than their healthy peers Therefore, it is important to identify, assess and understand the relevance of these comorbidities in order to characterize the full clinical spectrum of COPD and adjust prevention strategies, given the devastating consequences of these problems.

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“…In brain tissue, ROS are mostly generated by microglia and astrocytes, and they modulate synaptic and nonsynaptic communication between neurons and glia. 29 Many NPs, including ZnO NPs, can trigger damage to mitochondria and increase the mitochondrial membrane potential. [30][31][32] In the present study, a ROS assay was used to evaluate the change of the ROS level in BV-2 cells after exposure to 50 nm ZnO NPs.…”

mentioning

confidence: 99%

Involvement of PINK1/parkin-mediated mitophagy in ZnO nanoparticle-induced toxicity in BV-2 cells

Wei

Wang

Chen

et al. 2017

IJN

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With the increasing application of zinc oxide nanoparticles (ZnO NPs) in biological materials, the neurotoxicity caused by these particles has raised serious concerns. However, the underlying molecular mechanisms of the toxic effect of ZnO NPs on brain cells remain unclear. Mitochondrial damage has been reported to be a factor in the toxicity of ZnO NPs. PINK1/parkin-mediated mitophagy is a newly emerging additional function of autophagy that selectively degrades impaired mitochondria. Here, a PINK1 gene knockdown BV-2 cell model was established to determine whether PINK1/parkin-mediated mitophagy was involved in ZnO NP-induced toxicity in BV-2 cells. The expression of total parkin, mito-parkin, cyto-parkin, and PINK1 both in wild type and PINK1 −/− BV-2 cells was evaluated using Western blot analysis after the cells were exposed to 10 μg/mL of 50 nm ZnO NPs for 2, 4, 8, 12, and 24 h. The findings suggested that the downregulation of PINK1 resulted in a significant reduction in the survival rate after ZnO NP exposure compared with that of control cells. ZnO NPs were found to induce the transportation of parkin from the cytoplasm to the mitochondria, implying the involvement of mitophagy in ZnO NP-induced toxicity. The deletion of the PINK1 gene inhibited the recruitment of parkin to the mitochondria, causing failure of the cell to trigger mitophagy. The present study demonstrated that apart from autophagy, PINK1/parkin-mediated mitophagy plays a protective role in ZnO NP-induced cytotoxicity.

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ROS and Brain Diseases: The Good, the Bad, and the Ugly

Cited by 338 publications

References 173 publications

Influence of Chronic Coenzyme Q10 Supplementation on Cognitive Function, Learning, and Memory in Healthy and Diabetic Middle-Aged Rats

Influence of Chronic Coenzyme Q10 Supplementation on Cognitive Function, Learning, and Memory in Healthy and Diabetic Middle-Aged Rats

Neurocognitive Impairment as Systemic Effects of COPD

Involvement of PINK1/parkin-mediated mitophagy in ZnO nanoparticle-induced toxicity in BV-2 cells

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