Estrogen Prevents Neuroprotection by Caffeine in the Mouse 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Model of Parkinson's Disease

Xu, Kui; Xu, Yiling; Brown-Jermyn, Deborah; Chen, Jiang‐Fan; Ascherio, Alberto; Dluzen, Dean E.; Schwarzschild, Michael A.

doi:10.1523/jneurosci.3008-05.2006

Cited by 127 publications

(90 citation statements)

References 34 publications

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“…This question is particularly important since there are numerous reports of sex differences in the ability of caffeine to afford neuroprotection. For instance, there is an inverse association between caffeine intake and the incidence of Parkinson's disease, which is more evident in men than in women [72], possibly due to the interfering effect of estrogen replacement therapies [73], as also suggested in animal studies [74]. In contrast, the age-related cognitive decline was attenuated by caffeine consumption in women in one study [53], whereas another study reported an inverse association between caffeine intake and the risk of dementia that was stronger in men [56].…”

Section: Some Considerations For Future Studies Of Caffeine On Synaptmentioning

confidence: 77%

Caffeine, Adenosine Receptors, and Synaptic Plasticity

Costenla

Cunha

Mendonça

2010

JAD

112

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Abstract. Few studies to date have looked at the effects of caffeine on synaptic plasticity, and those that did used very high concentrations of caffeine, whereas the brain concentrations attained by regular coffee consumption in humans should be in the low micromolar range, where caffeine exerts pharmacological actions mainly by antagonizing adenosine receptors. Accordingly, rats drinking caffeine (1 g/L) for 3 weeks, displayed a concentration of caffeine of circa 22 µM in the hippocampus. It is known that selective adenosine A1 receptor antagonists facilitate, whereas selective adenosine A2A receptor antagonists attenuate, long term potentiation (LTP) in the hippocampus. Although caffeine is a non-selective antagonist of adenosine receptors, it attenuates frequency-induced LTP in hippocampal slices in a manner similar to selective adenosine A2A receptor antagonists. These effects of low micromolar concentration of caffeine (30 µM) are maintained in aged animals, which is important when a possible beneficial effect for caffeine in age-related cognitive decline is proposed. Future studies will still be required to confirm and detail the involvement of A1 and A2A receptors in the effects of caffeine on hippocampal synaptic plasticity, using both pharmacological and genetic approaches.

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Section: Some Considerations For Future Studies Of Caffeine On Synaptmentioning

confidence: 77%

Caffeine, Adenosine Receptors, and Synaptic Plasticity

Costenla

Cunha

Mendonça

2010

JAD

112

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“…The authors suggested that the protective effect of caffeine may be abrogated by postmenopausal estrogens [479], a theory supported by some experimental evidence [480].…”

Section: Coffee and Teamentioning

confidence: 94%

Epidemiology and etiology of Parkinson’s disease: a review of the evidence

et al. 2011

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“…It is therefore tenable that up-regulation of Cox activity by caffeine increases energy metabolism in the axon terminals of dopamine neurons, thereby protecting them from oxidative damage from such toxins. In support of this mechanism, caffeine has been shown to stimulate the opening of Kir6.2/SUR1 potassium channels (Mao et al, 2007), which has been shown to prevent neurons from depolarizing and releasing toxic levels of neurotransmitters (Avshalumov et al, 2005;Xu et al, 2006). By altering neuronal metabolism and enhancing the activity of potassium channels within the terminals of dopamine neurons in the striatum, caffeine may inhibit the excitotoxicity of these neurons, protecting them from degeneration.…”

Section: Cox Expression and Activity Is Stimulated By Caffeine 681mentioning

confidence: 98%

“…Six mice were sham-injected with vehicle, whereas the other six mice received an injection of caffeine (7.5 mg/kg). This dose of caffeine is on the low end of the physiologically relevant range (which is between 2 and 50 mg/kg) and is approximately equivalent to the concentration of caffeine (35 M) found in the human brain after consuming two cups of brewed coffee (Fredholm et al, 1999;Xu et al, 2006).…”

Section: Cox7c Protein Expression Is Up-regulated In Thementioning

confidence: 99%

Caffeine Stimulates Cytochrome Oxidase Expression and Activity in the Striatum in a Sexually Dimorphic Manner

et al. 2008

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Epidemiological studies indicate that caffeine consumption reduces the risk of Parkinson's disease (PD) in men, and antagonists of the adenosine 2A receptor ameliorate the motor symptoms of PD. These findings motivated us to identify proteins whose expression is regulated by caffeine in a sexually dimorphic manner. Using mass spectroscopy, we found that Cox7c, a nuclear-encoded subunit of the mitochondrial enzyme cytochrome oxidase, is up-regulated in the striatum of male but not female mice after receiving a single dose of caffeine. The expression of two other Cox subunits, Cox1 and Cox4, was also stimulated by caffeine in a male-specific fashion. This up-regulation of Cox subunits by caffeine was accompanied by an increase in Cox enzyme activity in the male striatum. Caffeine-induced stimulation of Cox expression and activity were reproduced using the adenosine 2A receptor (A2AR)-specific antagonist 5-amino-7-(2-phenylethyl)-2-(2-furyl)-pyrazolo[4,3-]-

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Estrogen Prevents Neuroprotection by Caffeine in the Mouse 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Model of Parkinson's Disease

Cited by 127 publications

References 34 publications

Caffeine, Adenosine Receptors, and Synaptic Plasticity

Caffeine, Adenosine Receptors, and Synaptic Plasticity

Epidemiology and etiology of Parkinson’s disease: a review of the evidence

Caffeine Stimulates Cytochrome Oxidase Expression and Activity in the Striatum in a Sexually Dimorphic Manner

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