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What Is The Relationship Between Caffeine And Parkinson’s Disease

Caffeine Modulates Neuroinflammation In Pd

56. Diet and Parkinsonâs disease: âWhatâs brewing?â?

The mechanisms underlying anti-neuroinflammation by caffeine may involve the antagonism of the A2AR, the major molecular target . A2ARs affords neuroprotection through the control of microglia reactivity and neuroinflammation. Notably, pharmacological blockade or genetic deletion of A2AR produces similar anti-neuroinflammatory and neuroprotective effects as with caffeine in several experimental models of PD . For example, enhanced reactive astrogliosis and NF-B p65 activation around the injection site in hippocampus in an -Syn transmission mouse model of PD, and these -Syn-triggered neuroinflammatory responses were largely prevented in A2AR KO mice . In the well-established -Syn fibril model of PD, chronic caffeine treatment largely reverted the -Syn-induced microglial activation and astrogliosis in the striatum in mice . Moreover, in A2AR antagonists also control neuroinflammation , of synaptopathy and -amyloid processing in AD models. Thus, caffeine may exert anti-neuroinflammation and neuroprotection effect in PD by targeting the A2ARs.

Smoking And Parkinsons Disease

Epidemiologic studies of Parkinsons disease that explore the distribution of the disease in various populations, have consistently found, over a number of decades, that cigarette smokers have lower rates of PD than non-smokers. People are taken aback when they first hear this as it is counter-intuitive. Could it be that a habit so clearly linked to poor health can also provide a health benefit?

There are two potential ways to view this association. The first is that smoking has a biological effect that protects a person from PD. The second is that part of the biology of PD makes it less likely that a person would smoke.

Does Smoking Protect From Parkinsons Disease

In addition to the numerous studies that demonstrate that PD rates are lower in cigarette smokers than the general population, there are studies that show that the inverse relationship between smoking and PD is dose-dependent. That is, the more a person smokes, the less of a chance that he or she will develop PD. Another study investigated identical twin pairs in which one had PD and the other did not. The twin without PD tended to smoke more than the twin with PD. Since identical twins share the same DNA and often the same environment, many of the variables normally associated with a difference in risk of PD were removed except for smoking. The study is therefore cited as evidence that smoking is protective against PD.

Even if this theory is correct, and smoking does protect people from Parkinsons disease, all physicians and researchers agree, that this does not mean that increasing the rates of smoking among the general population is a desirable strategy to prevent PD. That is because epidemiologic studies have also consistently found that cigarette smoking is a risk factor for a variety of deadly diseases including lung cancer, emphysema, heart disease and stroke. Researchers have therefore tried to harness the possibly protective nature of cigarette smoke in other ways.

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Efficacy Of Caffeine In Different People And Genders

Caffeine may show promise in the pharamcotherapy of PD since it antagonises adenosine receptors, inhibits the inflammatory response, and possibly inactivates calcium channels. The effect of caffeine was reported to be dose-dependent in a randomised controlled trial showing that a daily dose of 100-200mg of caffeine can reduce the risk of PD motor symptoms, while a daily dose of above 200mg caffeine was ineffective . The reason behind this discrepancy includes genetic variation and gender differences. Genetic variation in cytochrome CYP1A2 gives rise to fast and slow metabolisers of caffeine. CYP1A2 is a primary enzyme responsible for metabolism of 95% of caffeine into three active metabolites: paraxanthine, theophylline, and theobromine. Each of these metabolites exert different effects. Certain variations in CYP1A2 gene result in a reduced ability to metabolise caffeine slow metabolisers . These individuals are prone to hypertension as high levels of caffeine in serum can activate systemic epinephrine release. Moreover, sustained hypertension leads to vascular disease and possibly early myocardial infarction and cerebro-vascular accidents, that may then induce secondary neurodegenerative disorders such as vascular parkinsonism .

Mechanisms Of Neuroprotection By Caffeine In Pd

Is Coffee Good For Parkinson

Multiple mechanisms have been proposed to account for the neuroprotective effects of caffeine, including modulation of glutamatergic excitotoxicity and neuroinflammation via adenosine receptors . Furthermore, recent investigation into the autophagy and gut microbiota in PD pathogenesis raise the exciting possibilities that caffeine may modify autophagy and gut microbiome to influence PD development.

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Caffeine May Modulate Pd Pathology By Regulating Autophagy Activity

Using an -Syn fibril model of PD, we recently have provided the first evidence that caffeine can attenuate abnormal -Syn aggregation and neurotoxicity by re-establishing autophagy activity in animal models of PD . Specifically, chronic caffeine treatment did not affect autophagy processes in the normal mice striatum, but did selectively reverse -Syn-induced defects in macroautophagy and CMA . Thus, caffeine may represent a novel pharmacological therapy for PD by targeting autophagy pathway. This study collaborates with the previous study showing that caffeine-induced autophagy protected against human prion protein peptide -triggered apoptosis in a SH-SY5Y neuroblastoma cell line. Therefore, autophagy enhanced by caffeine may be a valid therapeutic strategy for neurodegenerative diseases such as PD and prion .

Comparison Between Coffee And Non

Of the 284 de novo PD patients enrolled , a total of 204 patients and 80 patients were categorized as coffee drinkers and non-coffee drinkers , respectively. The coffee drinker group comprised current coffee drinkers and those who have had coffee in the past but have now stopped. Most of the patients who quit drinking coffee had a history of coffee drinking for more than 10years. As shown in Table , intergroup comparisons revealed that coffee drinkers were younger, included more men, younger in age at cardinal motor symptom onset, and reported more years in formal education than the non-coffee drinkers. When comparing motor- and ADL-related scores, coffee drinkers had significantly lower UPDRS motor scores as well as tremor , bradykinesia , and gait and posture scores than non-coffee drinkers. When the tremor was divided into rest and action tremors, only rest tremor showed a significant difference. Furthermore, the univariate analysis revealed that coffee drinkers had significantly lower tremor scores than non-coffee drinkers. However, PIGD and AR scores were not significantly different between the two groups. When comparing non-motor scores, we found that coffee drinkers had higher MMSE , but lower BDI and total NMSS scores than non-coffee drinkers.

Table 1 Demographics and clinical characteristics of patients with Parkinsons disease

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Caffeine Has Been Found To Have Neuroprotective Effects In Patients With Parkinsons Disease

Study findings published in Neurology suggest that absolute lower levels of caffeine and caffeine metabolite profiles are promising diagnostic biomarkers for early Parkinsons Disease. This is consistent with the neuroprotective effect of caffeine previously revealed by epidemiologic and experimental studies.

A study of serum levels of caffeine in patients with Parkinsons Disease, published online in Neurology, found that serum levels of caffeine and 9 related metabolites were uniformly and significantly decreased in patients with Parkinsons Disease, despite an equivalent caffeine intake to controls. More importantly, serum levels of caffeine in patients with Parkinsons Disease related to caffeine intake significantly, but those in controls did more significantly, indicative of less caffeine absorption in patients with Parkinsons Disease.

There have been several reports suggesting an inverse association between daily caffeine consumption and a reduced risk of developing Parkinsons Disease in men, and in women not taking hormone replacement therapy, according to information cited in Neurology. Fujimaki M, Saiki S, Li Y, et al. Serum caffeine and metabolites are reliable biomarkers of early Parkinson disease. Neurology. 2018 Jan 3.

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Caffeine And Nicotine May Improve The Health Of Dopaminergic Systems

Neurodegenerative disorders. Part 2: Parkinson’s Disease
  • Christopher Martyn, clinical scientist,
  • Chris Gale, senior research fellow
  • MRC Environmental Epidemiology Unit, Southampton General Hospital, Southampton SO16 6YD
  • Parkinson’s disease belongs to that small group of conditions that occur less often among cigarette smokers than in non-smokers. The observation was first made in a case-control study over 30 years ago,1 but, as Hernán and colleagues have shown in their recent systematic review and meta-analysis,2 the finding has been replicated many times. The protective effect is largeaccording to the pooled data, current smokers have a 60% reduction in risk compared with those who have never smokedand consistent between studies in different settings. The fact that two very large prospective studies found a similar reduction in risk to that seen in retrospective studies rules out the possibility that the association can be accounted for by differential survival between smokers and non-smokers.3 Coffee drinking too, seems to protect against Parkinson’s disease. Here the pooled estimate is a 30% reduction in risk for coffee drinkers compared with non-drinkers.

    In An Essay on the Shaking Palsy,

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    Caffeine As A Biomarker For Parkinson’s Disease

    Researchers at Juntendo University report in Neurology the potential use of blood levels of caffeine and its byproducts as biomarkers for Parkinson’s disease. The finding is promising for the development of a method enabling early identification of the disease.

    Parkinson’s disease is a degenerative disorder of the central nervous system, affecting the latter’s motor systemthe part controlling bodily motion. Its symptoms include shaking, rigidity and difficulty with walking. There is evidence that daily caffeine consumption reduces the risk of developing Parkinson’s. Now, a team of researchers led by Nobutaka Hattori from Juntendo University School of Medicine have studied how traces of caffeine in the blood, after drinking coffee, can be indicative of Parkinson’s disease. The researchers found that caffeine levels are significantly lower in patients with the disease caffeine concentrations could therefore be used as an indicator of Parkinson’s, particularly in its early stages.

    The researchers studied a group of 139 people, both men and women, with and without Parkinson’s disease. Each person drank between 0 and 5 cups of coffee per day . Then, they checked the participants’ blood serum for traces of caffeine and its 11 so-called downstream metabolitessmall molecules produced during caffeine-induced metabolic processes in the human body.

    Parkinson’s disease

    Caffeine

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    Does Parkinsons Disease Protect From Smoking

    What if cigarette smoking does not actually confer a positive biological effect on the brain to protect from PD, but rather some aspect of PD biology leads to less of a tendency to smoke? Dopamine is the main addiction chemical in the brain, so it stands to reason that in a PD brain, with a reduced amount of dopamine, there will be less of a tendency for addiction. Other hypotheses suggest that people with PD may have alterations in how their brains utilize nicotine, or how the nicotine interacts with the dopaminergic neurons, leading to less of a tendency to become addicted to it.

    This possibility was explored in a paper that demonstrated that people with PD who did smoke found it easier to quit smoking as compared to controls, and people with PD utilized reduced amounts of nicotine substitutes in order to quit as compared to controls. This suggested that people with PD have a less intense addiction than controls, leading to the overall decreased smoking rates.

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    In the first comprehensive examination of caffeine consumption from a variety of sources and the risk of developing Parkinsons disease, researchers from the Harvard School of Public Health have determined that moderate consumption of caffeine reduces the risk of Parkinsons disease in men and women. The findings are published on the Web site for the Annals of Neurology at .

    Parkinsons disease is a progressive nervous disease occurring generally after age 50. It destroys brain cells that produce the chemical dopamine, lack of which leads to the muscular tremor, slowing of movement, weakness, and facial paralysis that characterize the disorder.

    Men who drank four to five cups per day of caffeinated coffee cut the risk of developing Parkinsons disease nearly in half compared with men in the study who consumed little or no caffeine daily. Women who consumed between one and three cups of caffeinated coffee per day also cut their risk of developing Parkinsons disease nearly in half when compared with women who drank less than a cup of coffee per day, but this apparent benefit was lost at higher levels of intake. Further research with women is required.

    The questionnaires contained inquiries on more than 100 food items among them were coffee with caffeine, tea , cola beverages, chocolate, decaffeinated beverages, and soft drinks with and without caffeine.

    Coffee Doesn’t Help Parkinson’s Motor Disorders

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    Caffeine has no impact, says long-term trial that reverses earlier findings

    HealthDay Reporter

    THURSDAY, Sept. 28, 2017 — Regular cups of coffee will not ease tremors and movement problems caused by Parkinson’s disease, despite prior evidence that caffeine might help, a new clinical trial reports.

    Earlier short-term results from the same trial had shown caffeine improved the motor function of a small group of Parkinson patients, researchers said.

    But long-term results from the trial now show that patients received no benefit from caffeine by six to 18 months after starting therapy, said lead researcher Dr. Ronald Postuma, an associate professor of neurology at McGill University Health Center in Montreal.

    “Caffeine made no difference to Parkinson’s,” Postuma said. “You can’t use it as a medication for Parkinson’s.”

    The findings will be disappointing for many Parkinson’s patients who turned to coffee to help their symptoms.

    The first results from the caffeine trial made a big splash in the media, despite the fact they reported the effects after only six weeks, Postuma said. They were published in the journal Neurology in 2012.

    “The news media picked it up, and all of a sudden I’ve got all of my patients drinking coffee, which I never intended,” Postuma said. “We always have to verify things.”

    That led Postuma and his colleagues to investigate whether these motor symptoms could be treated using one of the cheapest adenosine blockers available — caffeine.

    Neurology

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    Motor Benefit Of Caffeine In Pd Patients And Pd Models

    The symptomatic effect of caffeine in PD was first tested in 1970s , but has been revisited by several clinical studies recently. The motor benefit of caffeine were documented in a pilot open-label, 6-week dose-escalation study and a 6-week randomized controlled trial of caffeine involving 61 PD patients . These clinical studies suggest that caffeine improved objective motor deficits in PD with the reduced total Unified PD Rating Scale score and the objective motor component. Furthermore, coffee consumption is associated with the reduced hazard ratio for the development of dyskinesia compared with subjects who consumed < 112 mg/day in the Comparison of the Agonist Pramipexole with Levodopa on Motor Complications of Parkinsons Disease and CALM Cohort extension studies . Based on these positive findings, caffeine was recently investigated for motor and disease-modification involving 121 PD patients PD in a phase 3, 5-years , two-arm, double-blind RCT, with a primary outcome focused on motor symptoms and disease-modification as a secondary outcome1. Unfortunately, with the primary outcome analysis after 6 months demonstrating no significant symptomatic benefit of caffeine , the study was terminated earlier than the planned.

    Caffeine As An Adjuvant Therapy In Pd

    The evidence outlined above highlights a number of beneficial effects of caffeine that could possibly justify its use as an adjuvant drug in the management of PD. There are reported experimental uses of caffeine in treating PD. For instance, trihexyphenidyl is an anti-parkinsonian agent that has been clinically used to treat PD . It is a potent M1 receptor antagonist that inhibits M1 receptors in different parts of the cerebral cortex. Its use is accompanied by side effects that include memory impairment . When THP is co-administered with low doses of caffeine in mice, there is increased THP potency without memory impairment. Observational studies on reserpine-induced hypokinesia in rats reported no reversal of symptoms when caffeine or THP were used on their own . Conversely, when caffeine and THP were co-administered, they restored locomotion in reserpine-treated rats.

    The authors concluded that low doses of caffeine co-administered with THP might help reduce a number of motor deficiencies in animals, which are seen in PD. Nevertheless, long-term randomized clinical trials are needed to assess such claims and therapeutic benefits of such co-administration .

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    Astrocytes And Their Role In Pd

    Aside from being an A2A antagonist, caffeine may help stabilise the blood-brain barrier by regulating astrocytes and inflammatory processes in animal models . Astrocytes are glial cells found in the mammalian brain that play a pivotal role in maintaining various neuronal functions by transporting nutrients and metabolites to neurons through a number of transporters such as the malate-aspartate shuttle. There are two types of astrocytes found in substantia nigra: .

  • Protoplasmic astrocytes which encapsulate neuronal bodies and synapses
  • Fibrous astrocytes which interact with oligodendroglia and node of Ranvier
  • Research on astrocytes in mice has suggested that -synuclein affects only protoplasmic astrocytes but not fibrous astrocytes .

    Astrocytes are significant players in the central nervous system as they develop and maintain the BBB and promote neurovascular coupling. One extreme of astrocytes faces endothelial cells to maintain BBB and control cerebral blood flow while the other extreme is in communication with numerous neurons . Moreover, astrocytes can release chemokines, gliotransmitters and help in the uptake of glutamate and GABA from the synaptic cleft. Other functions of astrocytes include pH regulation, K+ buffering, metabolising dopamine, and producing antioxidants such as gluthathione and superoxide dismutases .

    3.2.1. Caffeine Inhibits Astrocyte-induced Inflammation in PD

    Caffeine May Influence Pd Pathology By Modulating Gut Microbiota

    Caffeine EXPOSED!!!

    The gut microbiota in the human gastrointestinal tract is estimated to contain 10 times more microbial cells than human cells, and approximately 100200-times more protein coding genes than the human genome . The gut microbiota critically influence various aspects of human biology, including the absorption and metabolism of nutrients, vitamins, medications, and toxic compounds the development and differentiation of the intestinal epithelium and immune system, the maintenance of tissue homeostasis, and the prevention of pathogens invasion . The gut microbiota also plays an important role in gut-brain communication, and the neuroimmune system to maintain brain homeostasis, thus influencing brain function and behavior . In healthy subjects, the intestinal microbiota is generally stable over time, but compositional changes might occur following antibiotic usage or dietary modifications .

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