Neuroprotection by caffeine and adenosine A<sub>2A</sub> receptor blockade of <i>β</i>‐amyloid neurotoxicity

Dall'Igna, Oscar Phelippe Permigotti; Porciúncula, Lisiane O.; Souza, Diogo O.; Cunha, Rodrigo A.; Lara, Diogo R.

doi:10.1038/sj.bjp.0705400

Cited by 52 publications

(78 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…No histopathological alterations in the hippocampus were shown upon treatment with caffeine in this study indicating its ability to prevent neuronal damage caused by AlCl 3 . Previous results showed that caffeine can prevent neuronal damage and cognitive deficit caused by Aβ, an effect mimicked by A 2A receptor antagonists [55].…”

Section: Discussionmentioning

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

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

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

View full text Add to dashboard Cite

show abstract

“…Research with mice showed that while drinking coffee, caffeine enters the bloodstream and acts as an antagonist on the A 2a adenosine receptors in the brain (Fredholm et al, 1999). Subsequently, this stimulates the secretion of cholinergic neurotransmitters (like acetylcholine), which in turn prevents b-amyloid-induced neurotoxicity in cerebellar neurons (Dall'Igna et al, 2003). Precise neuronal cellular mechanisms are not yet known and the generalizability of animal research to humans has its limitations.…”

Section: Discussionmentioning

confidence: 99%

“…A possible underlying mechanism could be that caffeine enters the bloodstream and acts as an antagonist on the A 2a adenosine receptors in the brain, which consequently stimulates cholinergic neurons (Fredholm et al, 1999). Subsequently, these neurons protect against b-amyloid-induced neurotoxicity, a precursor of cognitive decline (Dall'Igna et al, 2003). If coffee consumption could delay cognitive decline, this could have major public health implications because cognitive decline is very common in the elderly.…”

Section: Introductionmentioning

confidence: 99%

Coffee consumption is inversely associated with cognitive decline in elderly European men: the FINE Study

et al. 2006

View full text Add to dashboard Cite

Objective: To investigate whether coffee consumption is associated with 10-year cognitive decline in elderly men, as results of previous studies obtained hitherto have been controversial and prospective information on this association has been lacking. Design, subjects and setting: Six hundred and seventy six healthy men born between 1900 and 1920 from Finland, Italy and the Netherlands participated in a 10-year prospective cohort study. Cognitive functioning was assessed using the Mini-Mental State Examination (0-30 points, with a higher score indicating better cognitive performance). Coffee consumption was estimated in cups per day. A mixed longitudinal model was used to investigate the association between baseline coffee consumption and 10-year cognitive decline. Multiple adjustments were made. Results: Men who consumed coffee had a 10-year cognitive decline of 1.2 points (4%). Non-consumers had an additional decline of 1.4 points (Po0.001). An inverse and J-shaped association was observed between the number of cups of coffee consumed and cognitive decline, with the least cognitive decline for three cups of coffee per day (0.6 points). This decline was 4.3 times smaller than the decline of non-consumers (Po0.001). Conclusions: Findings suggest that consuming coffee reduces cognitive decline in elderly men. An inverse and J-shaped association may exist between the number of cups of coffee consumed and cognitive decline, with the least cognitive decline for men consuming three cups of coffee per day.

show abstract

“…In fact, both caffeine and antagonists of A 2A Rs (SCH 58261 or ZM 241385) effectively prevent the neurotoxicity induced by exposure of cerebellar [263] or hippocampal neurons [264] to the fragment 25Y35, 1Y40 or 1Y42 of b-amyloid protein (Ab), a putative causative factor of Alzheimer's disease [265]. And there is no evidence to suggest that Ab enhances glutamate release, since the effect of Ab is the opposite, i.e.…”

Section: A 2a Receptor Blockade Confers Robust Neuroprotectionmentioning

confidence: 99%

Neuroprotection by adenosine in the brain: From A1 receptor activation to A2A receptor blockade

Cunha

2005

Purinergic Signalling

482

432

View full text Add to dashboard Cite

Adenosine is a neuromodulator that operates via the most abundant inhibitory adenosine A 1 receptors (A 1 Rs) and the less abundant, but widespread, facilitatory A 2A Rs. It is commonly assumed that A 1 Rs play a key role in neuroprotection since they decrease glutamate release and hyperpolarize neurons. In fact, A 1 R activation at the onset of neuronal injury attenuates brain damage, whereas its blockade exacerbates damage in adult animals. However, there is a down-regulation of central A 1 Rs in chronic noxious situations. In contrast, A 2A Rs are up-regulated in noxious brain conditions and their blockade confers robust brain neuroprotection in adult animals. The brain neuroprotective effect of A 2A R antagonists is maintained in chronic noxious brain conditions without observable peripheral effects, thus justifying the interest of A 2A R antagonists as novel protective agents in neurodegenerative diseases such as Parkinson's and Alzheimer's disease, ischemic brain damage and epilepsy. The greater interest of A 2A R blockade compared to A 1 R activation does not mean that A 1 R activation is irrelevant for a neuroprotective strategy. In fact, it is proposed that coupling A 2A R antagonists with strategies aimed at bursting the levels of extracellular adenosine (by inhibiting adenosine kinase) to activate A 1 Rs might constitute the more robust brain neuroprotective strategy based on the adenosine neuromodulatory system. This strategy should be useful in adult animals and especially in the elderly (where brain pathologies are prevalent) but is not valid for fetus or newborns where the impact of adenosine receptors on brain damage is different.Abbreviations: Ab -b-amyloid peptide; A 1 Rs -A 1 receptors; A 2A Rs -A 2A

show abstract

Neuroprotection by caffeine and adenosine A_2A receptor blockade of β‐amyloid neurotoxicity

Abstract: British Journal of Pharmacology (2003) 139, 1571. doi:

Cited by 52 publications

References 0 publications

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

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

Coffee consumption is inversely associated with cognitive decline in elderly European men: the FINE Study

Neuroprotection by adenosine in the brain: From A1 receptor activation to A2A receptor blockade

Contact Info

Product

Resources

About

Neuroprotection by caffeine and adenosine A2A receptor blockade of β‐amyloid neurotoxicity

Abstract: British Journal of Pharmacology (2003) 139, 1571. doi:

Cited by 52 publications

References 0 publications

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

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

Coffee consumption is inversely associated with cognitive decline in elderly European men: the FINE Study

Neuroprotection by adenosine in the brain: From A1 receptor activation to A2A receptor blockade

Contact Info

Product

Resources

About

Neuroprotection by caffeine and adenosine A_2A receptor blockade of β‐amyloid neurotoxicity