Caffeine prevents age-associated recognition memory decline and changes brain-derived neurotrophic factor and tirosine kinase receptor (TrkB) content in mice

Costa, Marcelo Silveira da; Botton, Paulo Henrique S.; Mioranzza, Sabrina; Souza, Diogo O.; Porciúncula, Lisiane O.

doi:10.1016/j.neuroscience.2008.03.038

Cited by 105 publications

(65 citation statements)

References 68 publications

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“…Given that the rats used in our current study do not exhibit AD pathology but were rather a model of normal aging, this previous result is more in agreement with that of our current study in that it is not the caffeine in coffee that contributes to the improvements observed in performance. However, another study did show that 1 mg/mL of caffeine administered to male albino CF1 mice during adulthood for 12 months prevented age-associated decline in short-term recognition memory (Costa et al 2008), while Prediger and colleagues found that age-related deficits in olfactory discrimination and social recognition memory in rats were reversed by acute administration of caffeine (10.0 or 30.0 mg/kg, i.p. ), although this was just a single injection (Prediger et al 2005).…”

Section: Discussionmentioning

confidence: 98%

Coffee, but not caffeine, has positive effects on cognition and psychomotor behavior in aging

Shukitt‐Hale

Miller

Chu

et al. 2013

AGE

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The complex mixture of phytochemicals in fruits and vegetables provides protective health benefits, mainly through additive and/or synergistic effects. The presence of several bioactive compounds, such as polyphenols and caffeine, implicates coffee as a potential nutritional therapeutic in aging. Moderate (three to five cups a day) coffee consumption in humans is associated with a significant decrease in the risk of developing certain chronic diseases. However, the ability of coffee supplementation to improve cognitive function in aged individuals and the effect of the individual components in coffee, such as caffeine, have not been fully evaluated. We fed aged rats (19 months) one of five coffeesupplemented diets (0, 0.165, 0.275, 0.55, and 0.825 % of the diet) for 8 weeks prior to motor and cognitive behavior assessment. Aged rats supplemented with a 0.55 % coffee diet, equivalent to ten cups of coffee, performed better in psychomotor testing (rotarod) and in a working memory task (Morris water maze) compared to aged rats fed a control diet. A diet with 0.55 % coffee appeared to be optimal. The 0.165 % coffeesupplemented group (three cups) showed some improvement in reference memory performance in the Morris water maze. In a subsequent study, the effects of caffeine alone did not account for the performance improvements, showing that the neuroprotective benefits of coffee are not due to caffeine alone, but rather to other bioactive compounds in coffee. Therefore, coffee, in achievable amounts, may reduce both motor and cognitive deficits in aging.

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Section: Discussionmentioning

confidence: 98%

Coffee, but not caffeine, has positive effects on cognition and psychomotor behavior in aging

Shukitt‐Hale

Miller

Chu

et al. 2013

AGE

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“…This putative relevance of targeting A 2A Rs to control memory impairment associated with neurodegenerative conditions is strongly supported by the ability of caffeine to counteract the development of neurodegenerative conditions and, in particular, the development of cognitive deficits (for review, see Cunha, 2008b;Takahashi et al, 2008). In fact, although it is doubtful that caffeine is a cognitive enhancer, its long-term consumption is clearly associated with decreased memory impairment caused by different perturbing conditions (Cunha, 2008b;Takahashi et al, 2008) such as on aging (Ritchie et al, 2007;Costa et al, 2008a) or Alzheimer's disease (Maia and de Mendonça, 2002;Eskelinen et al, 2009). The only known mechanisms of action of nontoxic doses of caffeine are the antagonism of adenosine receptors (Fredholm et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Adenosine A_2AReceptor Blockade Prevents Synaptotoxicity and Memory Dysfunction Caused by β-Amyloid Peptides via p38 Mitogen-Activated Protein Kinase Pathway

Canas¹,

et al. 2009

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“…The beneficial effects exerted by caffeine on cognitive functions have been documented [18], and it was reported that caffeine consumption prevents memory disturbances associated with ageing [19,20,21]. Also, increasing attention has been given to caffeine since its intake has been associated with a reduced neurological damage in several neurodegenerative diseases [22].…”

Section: Caffeine: Potential Beneficial Effectsmentioning

confidence: 99%

Therapeutic Opportunities for Caffeine and A<sub>2A</sub> Receptor Antagonists in Retinal Diseases

Boia

Ambrósio²,

Santiago³

2016

Ophthalmic Res

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Caffeine, the major component of coffee, is the most consumed psychostimulant in the world. Caffeine is an adenosine analog and acts as a nonselective adenosine receptor antagonist. The majority of the effects of caffeine are mainly mediated by the blockade of adenosine receptors, and the proved neuroprotective effects of caffeine in brain disorders have been mimicked by the blockade of adenosine A_2A receptor (A_2AR). A growing body of evidence demonstrates that microglia-mediated neuroinflammation plays a key role in the pathophysiology of brain and retinal diseases. Moreover, the control of microglia reactivity by blocking A_2AR has been proposed to be the mechanism underlying the observed protective effects of caffeine. Hence, it is conceivable that caffeine and A_2AR antagonists offer therapeutic value for the treatment of retinal diseases, mainly those involving microglia-mediated neuroinflammation.

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Caffeine prevents age-associated recognition memory decline and changes brain-derived neurotrophic factor and tirosine kinase receptor (TrkB) content in mice

Cited by 105 publications

References 68 publications

Coffee, but not caffeine, has positive effects on cognition and psychomotor behavior in aging

Coffee, but not caffeine, has positive effects on cognition and psychomotor behavior in aging

Adenosine A_2AReceptor Blockade Prevents Synaptotoxicity and Memory Dysfunction Caused by β-Amyloid Peptides via p38 Mitogen-Activated Protein Kinase Pathway

Therapeutic Opportunities for Caffeine and A<sub>2A</sub> Receptor Antagonists in Retinal Diseases

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Caffeine prevents age-associated recognition memory decline and changes brain-derived neurotrophic factor and tirosine kinase receptor (TrkB) content in mice

Cited by 105 publications

References 68 publications

Coffee, but not caffeine, has positive effects on cognition and psychomotor behavior in aging

Coffee, but not caffeine, has positive effects on cognition and psychomotor behavior in aging

Adenosine A2AReceptor Blockade Prevents Synaptotoxicity and Memory Dysfunction Caused by β-Amyloid Peptides via p38 Mitogen-Activated Protein Kinase Pathway

Therapeutic Opportunities for Caffeine and A<sub>2A</sub> Receptor Antagonists in Retinal Diseases

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Adenosine A_2AReceptor Blockade Prevents Synaptotoxicity and Memory Dysfunction Caused by β-Amyloid Peptides via p38 Mitogen-Activated Protein Kinase Pathway