Caffeine induces beneficial changes in PKA signaling and JNK and ERK activities in the striatum and cortex of Alzheimer's transgenic mice

Zeitlin, Ross; Patel, Sagar P.; Burgess, Sarah; Arendash, Gary W.; Echeverrı́a, Valentina

doi:10.1016/j.brainres.2011.08.036

Cited by 75 publications

(72 citation statements)

References 52 publications

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“…Both PDE4 and PDE5 inhibition (Puzzo et al, 2009;Vecsey et al, 2009) and caffeine treatment (Zeitlin et al, 2011) increase CREB activity and can block the restorative action of melatonin on mitochondrial function as shown in this report. Melatonin can either stimulate or inhibit CREB activity depending upon the specific brain region studied.…”

Section: Mechanisms Through Which Caffeine May Block Melatonin Signalmentioning

confidence: 49%

Caffeine increases mitochondrial function and blocks melatonin signaling to mitochondria in Alzheimer's mice and cells

et al. 2012

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Section: Mechanisms Through Which Caffeine May Block Melatonin Signalmentioning

confidence: 49%

Caffeine increases mitochondrial function and blocks melatonin signaling to mitochondria in Alzheimer's mice and cells

et al. 2012

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“…It has been reported that induction of pCREB via PKA is important in N-methyl-D-aspartate receptor-mediated neuroprotection (24). Caffeine intake has been associated with a lower incidence of AD in humans, and it has been revealed that caffeine shifts the balance between neurodegeneration and neuronal survival towards the stimulation of pro-survival cascades and the inhibition of pro-apoptotic pathways in the striatum by increasing PKA and pCREB (25). In addition, several lines of evidence indicate that PKA/CREB are involved in Aβ-trigged disruption of synaptic plasticity in AD (26), and the overexpression of BACE1 reduces the activity of PKA and pCREB, contributing to the memory and cognitive deficits typical of AD (27).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-29c targets β-site amyloid precursor protein-cleaving enzyme 1 and has a neuroprotective role in vitro and in vivo

Yang

Song

Zhou

et al. 2015

Molecular Medicine Reports

103

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Abstract. Alzheimer's disease (AD), characterized by β-amyloid deposition and neurodegeneration, is the most common cause of dementia worldwide. Emerging evidence suggests that ectopic expression of micro (mi)RNAs is involved in the pathogenesis of AD. There is increasing evidence that miRNAs expressed in the brain are involved in neuronal development, survival and apoptosis. The expression of β-site amyloid precursor protein-cleaving enzyme 1 (BACE1) is regulated by dysregulated miRNAs in the brain. The present study determined the expression levels of the miRNA-29 (miR-29) family in peripheral blood samples of patients with AD and demonstrated a marked decrease in the expression of miR-29c compared with age-matched controls. In addition, a significant increase in the exprssion of BACE1 was observed in the peripheral blood of patients with AD. Correlation analysis revealed that the expression of miR-29c was negatively correlated with the protein expression of BACE1 in the peripheral blood samples from patients with AD. The present study also investigated the role of miR-29 on hippocampal neurons in vitro and in vivo. The results demonstrated that the upregulation of miR-29c promoted learning and memory behaviors in SAMP8 mice, at least partially, by increasing the activity of protein kinase A/cAMP response element-binding protein, involved in neuroprotection. This evidence suggested that miR-29c may be a promising potential therapeutic target against AD.

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“…A possible mechanism for the caffeine-induced effects is through the stimulation of pro-survival cascades and inhibition of pro-apoptotic pathways in the striatum and/or cortex, as shown in a recent study by Zeitlin et al (2011), where caffeine treatment in a transgenic model of AD was shown to stimulate PKA activity, to increase phospho-CREB levels and to decrease phospho-JNK and phospho-ERK expression in the striatum, all of which are thought to be beneficial changes for brain function. In the frontal cortex, caffeine did not significantly increase phospho-CREB and PKA activity but significantly reduced phospho-JNK and phospho-ERK expression in both transgenic and non-transgenic mice.…”

Section: Alzheimer's Diseasementioning

confidence: 95%

“…In the frontal cortex, caffeine did not significantly increase phospho-CREB and PKA activity but significantly reduced phospho-JNK and phospho-ERK expression in both transgenic and non-transgenic mice. These results suggest that caffeine promotes neuronal survival and reduces the process of neurodegeneration in the striatum and/or cortex, which may contribute to its beneficial effects against AD (Zeitlin et al, 2011). …”

Section: Alzheimer's Diseasementioning

confidence: 99%

Using caffeine and other adenosine receptor antagonists and agonists as therapeutic tools against neurodegenerative diseases: A review

2014

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Caffeine is the most consumed pychostimulant in the world, and it is known to affect basic and fundamental human processes such as sleep, arousal, cognition and learning and memory. It works as a nonselective blocker of adenosine receptors (A1, A2a, A2b and A3) and has been related to the regulation of heart rate, the contraction/relaxation of cardiac and smooth muscles, and the neural signaling in the central nervous system (CNS). Since the late 1990s, studies using adenosine receptor antagonists, such as Caffeine, to block the A1 and A2a adenosine receptor subtypes have shown to reduce the physical, cellular and molecular damages caused by a spinal cord injury (SCI) or a stroke (cerebral infarction) and by other neurodegenerative diseases such as Parkinson's and Alzheimer's diseases. Interestingly, other studies using adenosine receptor agonists have also shown to provide a neuroprotective effect on various models of neurodegenerative diseases through the reduction of excitatory neurotransmitter release, apoptosis and inflammatory responses, among others. The seemingly paradoxical use of both adenosine receptor agonists and antagonists as neuroprotective agents has been attributed to differences in dosage levels, drug delivery method, extracellular concentration of excitatory neurotransmitters and stage of disease progression. We discuss and compare recent findings using both antagonists and agonists of adenosine receptors in animal models and patients that have suffered spinal cord injuries, brain strokes, and Parkinson's and Alzheimer's diseases. Additionally, we propose alternative interpretations on the seemingly paradoxical use of these drugs as potential pharmacological tools to treat these various types of neurodegenerative diseases.

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Caffeine induces beneficial changes in PKA signaling and JNK and ERK activities in the striatum and cortex of Alzheimer's transgenic mice

Cited by 75 publications

References 52 publications

Caffeine increases mitochondrial function and blocks melatonin signaling to mitochondria in Alzheimer's mice and cells

Caffeine increases mitochondrial function and blocks melatonin signaling to mitochondria in Alzheimer's mice and cells

MicroRNA-29c targets β-site amyloid precursor protein-cleaving enzyme 1 and has a neuroprotective role in vitro and in vivo

Using caffeine and other adenosine receptor antagonists and agonists as therapeutic tools against neurodegenerative diseases: A review

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