Oxidative Stress and Neurodegenerative Disorders

Qureshi, G. Ali; Parvez, H.

doi:10.1016/b978-0-444-52809-4.x5140-0

Cited by 3 publications

(2 citation statements)

References 51 publications

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“…Neuroinflammation causes cognitive aging and increases the generation of reactive oxygen species (ROS), thus inducing oxidative stress [56,57]. Notably, oxidative stress is considered an underlying causative factor of neurodegenerative diseases [58]. NF-κB, c-Fos, and FosB are required for the transcription of inflammatory cytokines, such as ILs, and induce an inflammatory response [59,60].…”

Section: Cocainementioning

confidence: 99%

“…During cocaine withdrawal following chronic cocaine administration, mice showed memory deficits, especially in hippocampal-dependent memory, and increased basal c-Fos expression [63]. Glutamate is a major factor promoting oxidative stress in the brain, and excessive glutamate receptor activation can induce ROS generation through cell death [58,64]. In contrast, GABA and glutathione (GSH) inhibit nerve excitability and improve antioxidant capability [65].…”

Section: Cocainementioning

confidence: 99%

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Cellular messenger molecules mediating addictive drug-induced cognitive impairment: cannabinoids, ketamine, methamphetamine, and cocaine

Sim

Kim

2022

Futur J Pharm Sci

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Background Cognitive impairment is a commonly reported symptom with increasing life spans. Numerous studies have focused on identifying precise targets to relieve or reduce cognitive impairment; however, its underlying mechanism remains elusive. Most patients or animals exposed to addictive drugs exhibit cognitive impairment. Accordingly, the present review discusses the molecular changes induced by addictive drugs to clarify potential mechanisms that mediate cognitive impairments. Main body We investigated changes in cognitive function using four drugs: cannabinoids, ketamine, methamphetamine, and cocaine. Chronic administration of most addictive drugs reduces overall cognitive functions, such as working, spatial, and long-term recognition memories. Levels of several transcription factors involved in neuronal differentiation, as well as functional components of neurotransmitter receptors in neuronal cells, are reportedly altered. In addition, inflammatory factors showed a generally increasing trend. These impairments could be mediated by neuroinflammation, synaptic activity, and neuronal plasticity. Conclusion This review outlines the effects of acute or chronic drug use and potential molecular alterations in the central nervous system. In the central nervous system, addictive drug-induced changes in molecular pathways associated with cognitive function might play a pivotal role in elucidating the pathogenesis of cognitive impairment.

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Section: Cocainementioning

confidence: 99%

Section: Cocainementioning

confidence: 99%

Cellular messenger molecules mediating addictive drug-induced cognitive impairment: cannabinoids, ketamine, methamphetamine, and cocaine

Sim

Kim

2022

Futur J Pharm Sci

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Activity/inactivity circadian rhythm shows high similarities between young obesity-induced rats and old rats

Bravo

Delgado

Juánez

et al. 2016

Acta Physiologica Hungarica

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The objective of the present study was to compare differences between elderly rats and young obesity-induced rats in their activity/inactivity circadian rhythm. The investigation was motivated by the differences reported previously for the circadian rhythms of both obese and elderly humans (and other animals), and those of healthy, young or mature individuals. Three groups of rats were formed: a young control group which was fed a standard chow for rodents; a young obesity-induced group which was fed a high-fat diet for four months; and an elderly control group with rats aged 2.5 years that was fed a standard chow for rodents. Activity/inactivity data were registered through actimetry using infrared actimeter systems in each cage to detect activity. Data were logged on a computer and chronobiological analysis were performed. The results showed diurnal activity (sleep time), nocturnal activity (awake time), amplitude, acrophase, and interdaily stability to be similar between the young obesity-induced group and the elderly control group, but different in the young control group. We have concluded that obesity leads to a chronodisruption status in the body similar to the circadian rhythm degradation observed in the elderly.

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Alzheimer’s Disease and Antioxidant Therapy: How Long How Far?

Teixeira¹,

Silva²,

Andrade³

et al. 2013

CMC

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Alzheimer's disease (AD) has become a health problem to societies worldwide affecting millions of people. AD normally ensues in middle and late life but its specific cause remains unknown. Besides amyloid-β deposition and hyperphosphorylated tau protein, increased production of reactive species (RS) has also been described to be a hallmark in early steps of this disorder. Antioxidant therapy has received considerable attention over the last years as a promising approach to delay or slow the neurodegeneration progression in AD either by boosting the pool of endogenous antioxidants (e.g.vitamins, coenzyme Q10 or melatonin) or by the intake of dietary antioxidants, such as phenolic compounds of flavonoid or non-flavonoid type. However, the majority of antioxidants studied so far have limited success in clinical trials, a fact that could be related to their poor distribution and with the inherent difficulties to cross the blood brain barrier and attain the target sites. Despite the evidence that different classes of antioxidants are neuroprotectants in vitro, the clinical data is not consistent. Alzheimer's disease and antioxidant therapy is still an open question: the research is far from the end but the success may not be so time-consuming if the data obtained so far are gathered and rationally analyzed either by checking new targets or by the obtention of new and effective compounds, for instance by the rational modification of the previous ones.

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Oxidative Stress and Neurodegenerative Disorders

Cited by 3 publications

References 51 publications

Cellular messenger molecules mediating addictive drug-induced cognitive impairment: cannabinoids, ketamine, methamphetamine, and cocaine

Cellular messenger molecules mediating addictive drug-induced cognitive impairment: cannabinoids, ketamine, methamphetamine, and cocaine

Activity/inactivity circadian rhythm shows high similarities between young obesity-induced rats and old rats

Alzheimer’s Disease and Antioxidant Therapy: How Long How Far?

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