Chronic caffeine consumption prevents cognitive decline from young to middle age in rats, and is associated with increased length, branching, and spine density of basal dendrites in CA1 hippocampal neurons

Vila-Luna, S.; Cabrera-Isidoro, S.; Vila-Luna, L.; Juárez-Díaz, Ismael; Bata-García, José L.; Álvarez-Cervera, Fernando J.; Zapata-Vázquez, Rita Esther; Arankowsky‐Sandoval, Gloria; Heredia-López, Francisco J.; Flores, Gonzalo; Góngora-Alfaro, José L.

doi:10.1016/j.neuroscience.2011.11.053

Cited by 65 publications

(41 citation statements)

References 52 publications

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“…That caffeine is able to interfere with the trajectory of brain morphological changes during development has been shown previously. For example, caffeine was shown to have a long lasting effects on morphological parameters such as dendritic length in the neonatal rat in the prefrontal cortex [58] as well as in the middle age rat in the hippocampus preventing cognitive decline [59]. Knockout models may help to explore the underlying mechanism of a potential role of adenosine signalling during cortical maturation.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Caffeine on Sleep and Maturational Markers in the Rat

2013

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Adolescence is a critical period for brain maturation during which a massive reorganization of cortical connectivity takes place. In humans, slow wave activity (<4.5 Hz) during NREM sleep was proposed to reflect cortical maturation which relies on use-dependent processes. A stimulant like caffeine, whose consumption has recently increased especially in adolescents, is known to affect sleep wake regulation.The goal of this study was to establish a rat model allowing to assess the relationship between cortical maturation and sleep and to further investigate how these parameters are affected by caffeine consumption. To do so, we assessed sleep and markers of maturation by electrophysiological recordings, behavioral and structural readouts in the juvenile rat. Our results show that sleep slow wave activity follows a similar inverted U-shape trajectory as already known in humans. Caffeine treatment exerted short-term stimulating effects and altered the trajectory of slow wave activity. Moreover, caffeine affected behavioral and structural markers of maturation. Thus, caffeine consumption during a critical developmental period shows long lasting effects on sleep and brain maturation.

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Section: Discussionmentioning

confidence: 99%

The Effects of Caffeine on Sleep and Maturational Markers in the Rat

2013

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“…Five groups of rats (8/group) were used and received daily for five weeks: Saline for control group, AlCl 3 (70 mg/kg, IP) for AD group [22], while treated groups received together with AlCl 3 , either Caffeine (5 mg/kg, IP) [23], Nicotine (1 mg/kg, SC) [24] or both Caffeine and Nicotine. All drugs were administered at a dose volume 0.5 ml/250 g body weight.…”

Section: Experimental Designmentioning

confidence: 99%

The Potential Effect of Caffeine and Nicotine Co-administration against Aluminum-induced Alzheimer's disease in Rats

Ali¹,

Ahmed²

2016

J Alzheimers Dis Parkinsonism

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Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized clinically by cognitive decline and memory loss. Caffeine and nicotine are the most commonly co-used psycho stimulants. Caffeine is one of the major contributors to the dietary antioxidants which prevent oxidative damage and may reduce the risk of chronic neurodegenerative diseases. Nicotine has the ability to decrease level of reactive oxygen species (ROS) in the hippocampus and suggested to attenuate the impairment of memory associated with AD. The study aimed to evaluate the influence of caffeine and nicotine co-administration against aluminium-induced neurotoxicity that mimics AD in rats. Five groups of rats were used and received daily for five weeks: Saline for control, aluminium chloride (AlCl 3 ) (70 mg/kg, IP) for AD mimic group, while treated groups received together with AlCl 3 , either Caffeine (5mg/kg, IP), Nicotine (1 mg/kg, SC) or their combination. Three behavioral experiments were performed: Forced Swimming Test (FST), Morris Water Maze (MWM) task and Conditioned-Avoidance and Learning (CAL) test. Histo pathological changes in the brain and biochemical changes in Acetyl cholinesterase (AchE) as well as oxidative parameters; malon dialdehyde (MDA), superoxide dismutase (SOD), total anti oxidane capacity (TAC) were also evaluated for all groups. Results of the behavioral tests showed that caffeine and nicotine co-administration had more pronounced protecting effect from learning and memory impairment induced by AlCl 3 than each one alone. Caffeine and nicotine co-administration also prevent neuronal degeneration in the hippocampus and the eosinophilic plagues in the striatum induced by AlCl 3 while nicotine alone still showed mild gliosis in striatum. The marked protection of caffeine and nicotine co-administration confirmed also by the significant increase in TAC and SOD and decrease in MDA and AchE in brain tissue. In conclusion, co-administration of caffeine and nicotine can reduce the risk of neuronal degeneration in the hippocampus and attenuate the impairment of learning and memory associated with AD.

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“…Therefore, there is a need to rely on animal studies and observational epidemiologic studies of natural experiments in man to provide knowledge on the relationship between beverage consumption and decline. Animal studies do suggest that chronic caffeine consumption may prevent cognitive decline in male rats (2). Caffeine-treated rats given 5 mg/(kg $ d) for 6 mo outperformed a tap water control group on maze-based cognition tests conducted 2-3 wk after caffeine withdrawal.…”

Section: Introductionmentioning

confidence: 98%

Epidemiologic Evidence of a Relationship between Tea, Coffee, or Caffeine Consumption and Cognitive Decline

Arab

Khan

Lam

2013

Advances in Nutrition

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A systematic literature review of human studies relating caffeine or caffeine-rich beverages to cognitive decline reveals only 6 studies that have collected and analyzed cognition data in a prospective fashion that enables study of decline across the spectrum of cognition. These 6 studies, in general, evaluate cognitive function using the Mini Mental State Exam and base their beverage data on FFQs. Studies included in our review differed in their source populations, duration of study, and most dramatically in how their analyses were done, disallowing direct quantitative comparisons of their effect estimates. Only one of the studies reported on all 3 exposures, coffee, tea, and caffeine, making comparisons of findings across studies more difficult. However, in general, it can be stated that for all studies of tea and most studies of coffee and caffeine, the estimates of cognitive decline were lower among consumers, although there is a lack of a distinct dose response. Only a few measures showed a quantitative significance and, interestingly, studies indicate a stronger effect among women than men.

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Chronic caffeine consumption prevents cognitive decline from young to middle age in rats, and is associated with increased length, branching, and spine density of basal dendrites in CA1 hippocampal neurons

Cited by 65 publications

References 52 publications

The Effects of Caffeine on Sleep and Maturational Markers in the Rat

The Effects of Caffeine on Sleep and Maturational Markers in the Rat

The Potential Effect of Caffeine and Nicotine Co-administration against Aluminum-induced Alzheimer's disease in Rats

Epidemiologic Evidence of a Relationship between Tea, Coffee, or Caffeine Consumption and Cognitive Decline

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