Top 10 Parkinson’s Stories of 2019

Top 10 stories on Parkinson's

Parkinson’s News Today keeps you up-to-date with research into Parkinson’s disease as it emerges. We brought you daily coverage of experiments into the basic biology of Parkinson’s, results of clinical and pre-clinical trials, and key findings from Parkinson’s research around the globe.

We look forward to bringing more such news to those with Parkinson’s, their family, friends and caregivers throughout 2020.

Here are our 10 most-read stories of 2019, with a short summary of what makes each one relevant to the Parkinson’s community.

No. 10 – “Active Form of Vitamin B12 Found to Prevent Neurodegeneration in Study of Animal Models

A study found that an active form of the vitamin B12 called AdoCbl can ease the effects of dopamine loss that occurs in Parkinson’s disease. Using cell lines and several animal models, researchers showed that by reducing LRRK2 enzyme activity, AdoCbl limits the death of dopamine-producing nerve cells, thereby preventing the appearance of symptoms associated with neurodegeneration. Overactivity of LRRK2 is linked to the development of a hereditary form of Parkinson’s.  AdoCbl is already an FDA-approved compound, and “could be used as a basis to develop new therapies to combat hereditary Parkinson’s associated with pathogenic variants of the LRRK2 enzyme,” according to Iban Ubarretxena, director of the Biofisika Institute and a study co-author.

No. 9 – “Onstryv Now Approved for Parkinson’s Patients in Canada

Canadian Parkinson’s disease patients now have access to Onstryv (safinamide), also known as Xadago. Onstryv increases the amount of active dopamine in the brain by both preventing the enzyme that breaks dopamine down from doing so, and by blocking that enzyme from entering cells. Other available treatments cause debilitating fluctuations between normal motor function (called “on episodes”) and poorer motor function (“off periods”) as their effects ebb and flow. Four placebo-controlled Phase 3 trials showed that the combination of Onstryv and levodopa led to more “on” and fewer “off” periods, and improved motor function in patients. “The approval of [Onstryv] in Canada is a step forward for patients who need new treatment options for Parkinson’s disease,” said Roberto Tascione, CEO of Zambon, one of the companies involved in commercializing this medication.

Xadago was approved by the U.S. Food and Drug Administration in March 2017 to improve motor function in Parkinson’s patients who experience “off periods” while on treatment with levodopa and/or Lodosyn (carbidopa).

No. 8 – “Plant Antioxidant Seen to Aid Mitochondria and Ease Motor Problems in Early Parkinson’s Study

A pre-clinical study conducted in China showed that alpha-arbutin, an antioxidant found in plants such as the blueberry, might restore mitochondrial function in nerve cells and ease the motor disabilities associated with Parkinson’s disease. Treatment with alpha-arbutin partially restored mitochondrial function in nerve cells undergoing oxidative stress (mitochondria act as a cell’s power house). It also restored these cells’ ability to remove toxic waste products. Feeding alpha-arbutin to flies carrying a mutated gene known to trigger Parkinson’s significantly eased several Parkinson’s-like symptoms. “Naturally derived-antioxidants might serve as a new class of therapeutic options for [Parkinson’s disease],” the researchers wrote.

No. 7 – “Stem Cell Transplants Could Significantly Improve Parkinson’s Treatment, Study Suggests

Replacing damaged cells in Parkinson’s disease with dopamine-producing stem cells could ease motor symptoms and reduce or eliminate the need for pharmaceutical medicines. As current disease therapies lose their efficacy over time, stem cell therapy might “revolutionize” Parkinson’s treatment, its researchers said. “A single surgery could potentially provide a transplant that would last throughout a patient’s lifespan, reducing or altogether avoiding the need for dopamine-based medications,” said Claire Henchcliffe MD, PhD, and Malin Parmar, PhD, co-authors of a study on the benefits of stem cell therapy. However, “there are several biological, practical, and commercial hurdles that need circumventing for this to become a routine therapy,” according to the editors of the Journal of Parkinson’s Disease.

No. 6 – “Bacteria in Gut Can Promote Parkinson’s by Altering Brain’s Immune Reactions, Study Says

A study found evidence of interaction between the brain and the gut in Parkinson’s, in which Gram-negative bacterial infections in the gut trigger an immune response that damages nerve cells. Gut microorganisms are known to communicate with the central nervous system, and studies suggest that harmful proteins related to Parkinson’s may spread to the brain from the gut. Scientists at the Université de Montréal showed that Gram-negative bacteria, particularly those related to gut infections, triggered an immune response in cells taken from mice. They then showed that mice bred without the PINK1 gene (making them resistant to Parkinson’s-like symptoms), when infected with these bacteria, displayed an immune response that led to such symptoms. Mutations in the PINK1 gene cause damage to the mitochondria in brain cells, and are linked to early onset hereditary Parkinson’s. The work provides evidence that intestinal infection acts as a triggering event in Parkinson’s, and highlighted the relevance of a gut-brain connection in this disease.

No. 5 – “Next 20 Years Expected to Bring ‘Message of Hope’ to Parkinson’s Patients, Review Study Finds

By reviewing the past 20 years of research into Parkinson’s disease, two scientists see a strong potential for breakthroughs in how this disease is approached over the next 20 years. The review cited developments in better animal models, greater understanding of molecular mechanisms and risk factors, and advances in available and potential therapies as reasons for hope. Among highlights of many advances listed are: 1) the adaptation of existing medicines used in other diseases to treat Parkinson’s (drug repurposing); 2) targeting non-motor features such as cognition, speech and balance difficulties that often precede motor symptoms; 3) the use of nanoparticles to block the formation of toxic alpha-synuclein clusters; and, 4) emerging evidence of a link between harmful gut bacteria and brain inflammation. The review also stressed the importance of future trials to test combination therapies.

No. 4 – “Physical Activity, Coffee, Moderate Alcohol Consumption Protect Against Disease Progression, Study Reports

Good news for lovers of sports, caffeine, and happy hours — all of these things, in moderation, may help slow the onset of symptoms of Parkinson’s disease. Although how exactly these lifestyle factors affect disease progression remains poorly understood, they correlate strongly with better patient outcomes. Conversely, smoking, heavy drinking and no consumption of alcohol at all were linked to considerably worse outcomes. The study, published in the journal Movement Disorders, needs to be replicated to strengthen the usefulness of its findings. Nonetheless, the work “suggests that multiple lifestyle factors potentially modify the rate of symptom progression,” its researchers wrote.

No. 3 – “Dietary Supplement Eases Parkinson’s Symptoms, Improves Dopamine Function, Study Shows

The antioxidant dietary supplement N-acetyl-cysteine (NAC) may improve dopamine function and ease Parkinson’s disease symptoms, according to one study. The body uses NAC to produce an antioxidant called glutathione (GSH), which it uses to prevent the oxidative stress that leads to cell death. Damage due to oxidative stress within dopamine-producing neurons is a key clinical feature of Parkinson’s. A trial (NCT02445651), conducted by researchers at Thomas Jefferson University in Philadelphia, showed that NAC supplementation significantly eased both motor and non-motor symptoms among 42 Parkinson’s patients (21 men and 21 women). These results need to be confirmed in larger and placebo-controlled studies, but offer an encouraging start to a potential low-cost therapy.

No. 2 – “Low Vitamin D Levels Linked to Added Falls, More Sleep Problems, Depression, Study Shows

Low levels of vitamin D were associated with more falls, and greater problems with insomnia, anxiety, and depression in people with Parkinson’s disease, according to a study by Chinese researchers. Vitamin D deficiency has often been seen in people with Parkinson’s, but its relationship to the disease remains controversial. This study, by researchers at the Second Affiliated Hospital of Soochow University and Soochow University, is one of the few to measure both motor and non-motor outcomes. By conducting detailed clinical evaluations in 182 Parkinson’s patients, as well as 185 healthy controls, the group found that low levels of vitamin D were more common in Parkinson’s patients than in healthy people, and that vitamin D supplements may ease the disease’s non‐motor symptoms.

No. 1 – “Oral Magnesium Compound Able to Reach Brain Seen to Slow Motor Decline, Neuronal Loss in Early Study

Our year’s most-read story was of an early stage study reporting that a type of oral magnesium could enter the brain and ease motor symptoms and nerve cell loss in a mouse model of Parkinson’s disease. Mice given magnesium-L-threonate, which can cross the blood-brain barrier (a semipermeable membrane that protects the brain from the outside environment) reduced the loss of dopamine-producing neurons, slowed the decline in motor function, and limited the oxidative stress that is associated with Parkinson’s. It is important to note that while magnesium-L-threonate provided therapeutic benefits, magnesium sulfate — the first choice as a clinical magnesium supplement — did not. “[T]he combination of [magnesium] with an agent that promotes its transportation to the brain is essential for the neuroprotection of this element,” the study’s scientists wrote.


At Parkinson’s News Today we hope these stories and our reporting throughout 2020 help to better inform and improve the lives of everyone affected by Parkinson’s.

We wish all our readers a happy 2020.

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Migraines, OCD, and Seasonal Allergies May be Risk Factors for Parkinson’s, Large Study Suggests

Parkinson's traits

Migraines, obsessive-compulsive disorder, and seasonal allergies seem to be associated with Parkinson’s disease and are likely to occur many years before the typical age of diagnosis, a large study has found.

Results of the study, “The Parkinson’s phenome—traits associated with Parkinson’s disease in a broadly phenotyped cohort,” were published in the journal npj Parkinson’s Disease.

Trying to identify the factors that influence whether a person will develop Parkinson’s disease is not a new idea. However, because Parkinson’s is a rare disease, such studies often don’t have enough participants to be sure that associations are real and not the result of chance.

To try to get around this problem, researchers behind a new study analyzed data from 13,546 Parkinson’s patients and more than one million control subjects to find traits associated with Parkinson’s development.

The team primarily used data from customers of 23andMe — a web-based company that provides genetic testing and analysis — who consented to be included in the study, and from surveys sent to and filled by various Parkinson’s patient groups.

After amassing the data, the researchers set about finding the factors — including family history, other diagnoses, environmental factors, personality traits, and medication usage — that were correlated with developing Parkinson’s.

The team analyzed 832 traits individually, since not every patient had data for every trait. This resulted in a list of a few hundred traits that showed some evidence of an association with Parkinson’s. The researchers then applied statistical tests and corrected for factors such as education and income, and ended up with 122 traits that were significantly associated with the disease, including some previously known factors. For example, people who consumed a lot of caffeine were less likely to have Parkinson’s, and those with the disease were more likely to report experiencing constipation.

The researchers also identified 42 traits that had not previously been associated with Parkinson’s. For example, those who could wiggle their ears or whistle were less likely to have the disease, whereas Parkinson’s patients were more likely to be afraid of heights, be farsighted, have seasonal allergies, and be married.

This large study was able to shed light on associations that had been suggested but for which there hadn’t been large enough sample sizes to draw a definitive connection. For example, the investigators found that those with obsessive-compulsive disorder (OCD) were more likely to develop Parkinson’s, supporting previous studies that were too small to achieve significance.

Although previous studies have yielded non-significant results due to their small sample sizes, “with 10,437 (Parkinson’s) cases in this particular regression, our study was well-powered to detect a positive association between (Parkinson’s) and OCD,” the researchers stated.

In addition, they found a significant association between Parkinson’s and migraines.

“We observed that migraine was positively associated with (Parkinson’s),” they said. “Only two cohort studies have previously been conducted, but both found that midlife migraine was associated with increased risk of (Parkinson’s disease) …. Since the average age of onset is typically much earlier for migraine than for (Parkinson’s), migraine may be a novel (Parkinson’s) risk factor.”

While previous studies have shown that Parkinson’s was positively associated with allergic rhinitis, but not asthma or hayfever, the current study found that it was also associated with allergies to plants and antibiotics, but not with allergies to food or animals.

“Understanding the biological differences between these different groups of allergies may allow us to hone in on specific immunological pathways that contribute to (Parkinson’s) risk,” the researchers said. “Seasonal allergies typically develop early in life, but further research is needed to determine whether having seasonal allergies is a risk factor for (Parkinson’s). If so, it may be possible to manipulate risk using immune-modulating drugs.”

The researchers noted that their study showed correlations, and not causation — that one thing does not necessarily cause another because the two are correlated. For example, people with Parkinson’s tend to report being more introverted, but it’s highly debatable whether the factors that make a person introverted also predispose them to Parkinson’s or if people with Parkinson’s are more likely to become introverted due to the difficulties of living with a neurodegenerative disease.

Similarly, marital status doesn’t seem likely to influence the development of Parkinson’s, although the researchers noted that spouses may notice sleep disturbances, which could increase the chances of people eventually getting diagnosed. At this point, however, these ideas are largely speculation.

Still, this study is not without value: “Now that we have identified phenotypes (traits) that are correlated with (Parkinson’s) it is also possible to test whether these phenotypes are causes or consequences of the disease,” the investigators wrote, adding that even in the absence of a known causal relationship, “phenotypes that are correlated with (Parkinson’s) can be used to predict (the disease) as long as the phenotype is enriched in (Parkinson’s disease) cases prior to diagnosis.”

In other words, having the data about factors that are associated with Parkinson’s can be a starting point for further research. It could be used to make predictions about Parkinson’s patients, particularly through the use of computer models and machine learning, which can interpret these massive datasets more efficiently than people.

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Mouse Studies Suggest Protective Effects of Caffeine in Parkinson’s Disease

caffeine and Parkinson's

Two new studies in mice suggest that caffeine might have protective effects in the brains of Parkinson’s disease patients.

The studies, “Chronic Caffeine Treatment Modulates  Disease Progression in a Transgenic Alpha-Synuclein Prion-Like Spreading Mouse Model of Parkinson’s Disease,” and “Chronic Caffeine Treatment Reverses A-Synuclein-Induced Cognitive Impairment With Enhanced Dendritic Spine Density and Morphology in Mice,” will be presented during the 14th​ International Conference on Alzheimer’s and Parkinson’s Diseases and related neurological disorders, March 26-31 in Lisbon, Portugal.

Previous epidemiological studies have suggested that consuming caffeine might protect against the development of Parkinson’s. These more-recent studies set out to test this premise more directly in an animal model.

Both studies used mouse models of Parkinson’s that involved injecting mice with alpha-synuclein. This protein is a major component of Lewy bodies, irregular “clumps” in brain cells that are a hallmark of Parkinson’s pathology. Specifically, both research teams used a mutant form of the protein called A53T, which forms these clumps even more effectively than the wild-type protein.

In both studies, injection with A53T led to changes characteristic of Parkinson’s disease, such as impaired motor function and memory, as well as changes in brain physiology, like the development of the aforementioned Lewy bodies and loss of dendritic spines (parts of neurons involved in making connections in the brain).

However, when the mice were given caffeine in their drinking water, these effects were lessened. Both studies showed similarly beneficial results, though the exact parameters that were measured were different.

In the first study, researchers at Aarhus University, Denmark, report that mice given caffeine had less alpha-synuclein in their brains. Caffeine also caused a three–week delay in the onset of clasping, which is a behavior mice do with their hind limbs that is indicative of brain damage. Furthermore, caffeine-treated mice lived, on average, 40% longer than their counterparts who weren’t given caffeine.

In the second study, researchers at Wenzhou Medical University, China, reported that mice given caffeine had fewer memory problems and more dendritic spines than their untreated counterparts.

Both studies support the previous epidemiological evidence that caffeine can be protective for Parkinson’s disease, although there is the usual caveat that experiments in animal models are never a perfect replica of actual human disease.

It also is not clear why or how caffeine might have such protective effects, and further research will be needed to figure out just how caffeine might benefit Parkinson’s patients.

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Caffeine Plus Coffee Compound Linked to Serotonin Help Protect Brain from Toxic Damage, Mouse Study Says

coffee and its compounds

Two compounds found in coffee — caffeine and EHT, a fatty acid molecule derived from serotonin — work together to protect the brain from damage induced by alpha-synuclein, a study in mice reported.

The study, “Synergistic neuroprotection by coffee components eicosanoyl-5-hydroxytryptamide and caffeine in models of Parkinson’s disease and DLB,” was published in PNAS.

Parkinson’s disease is characterized by alpha-synuclein aggregates. When this protein clumps, it gives rise to small fibrils that accumulate inside brain cells, producing small inclusions called Lewy bodies. These structures are highly toxic and often cause irreparable damage to affected nerve cells, slowly killing them.

Previous studies have shown that alpha-synuclein is abnormally hyperphosphorylated — a chemical modification in which a phosphate group is added to the protein — in the brain of patients with Parkinson’s. This is caused by the lack of activity of the protein phosphatase 2A (PP2A), an enzyme responsible for removing phosphate groups from alpha-synuclein.

Of note, alpha-synuclein phosphorylation is known to occur in Parkinson’s disease, and is thought to be a critical step in disease progression as it enhances alpha-synuclein’s toxicity —possibly by increasing the formation of alpha synuclein aggregates.

Interestingly, studies also report that Eicosanoyl-5-hydroxytryptamide or EHT — a fatty acid molecule found in coffee — promotes the activation of PP2A. In transgenic (or genetically engineered) mice, it was able to reverse the symptoms of phosphorylation to produce large quantities of alpha-synuclein.

The chemical serotonin, a neurotransmitter, is known to serve as a “feel-good” chemical in the brain, influencing a person’s sense of well-being and happiness.

“Considering epidemiologic and experimental evidence suggesting protective effects of CAF [caffeine] in PD [Parkinson’s disease], we sought, in the present study, to test whether there is synergy between EHT and caffeine in models of [alpha]-synucleinopathy,” the researchers wrote.  “[A]mong patients with early PD, the amount of CAF consumption does not impact the rate of progression of the disease, and decaffeinated coffee has been found to be protective in Drosophila models of PD, raising some question about the protective effect of only CAF among the numerous other compounds in coffee.”

Researchers treated alpha-synuclein transgenic mice (SynTg) — which overexpress alpha-synuclein in nerve cells — with either higher doses of caffeine and EHT separately, or with lower doses of both compounds for six months.

SynTg mice treated with caffeine and EHT had lesser accumulation of hyperphosphorylated alpha-synuclein in the brain, which was linked to higher levels of active PP2. These animals also  maintained neuron integrity and function, had lower brain inflammation, and performed better on behavioral tests.

Investigators found the same therapeutic benefits when they used the combined treatment in another mouse model of alpha-synucleinopathy, in which animals were injected with pre-formed fibrils of alpha-synuclein (alpha-Syn PFF).

In both animal models, however treatment with either caffeine or EHT alone failed to produce the same positive effects.

“These findings suggest that these two components of coffee have synergistic effects in protecting the brain against [alpha]-synuclein−mediated toxicity through maintenance of PP2A in an active state,” the researchers wrote.

“As we begin to unravel the polypharmacology of the micronutrients in commonly consumed botanical extracts such as coffee, it seems likely that it will be possible to optimize their composition to enhance efficacy so as to provide widely available, inexpensive, and effective therapeutics for the prevention and treatment of neurodegenerative diseases such as PD, DLB [dementia with Lewy bodies], PSP [progressive supranuclear palsy], and AD [Alzheimer’s disease],” they concluded.

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Certain Compounds in Coffee, But Not Caffeine, Seen to Prevent Protein Buildup Linked to Parkinson’s in Early Study

coffee consumption

Chemical compounds in coffee — especially phenylindanes that form during the roasting of coffee beans — appear to prevent the damaging aggregation of amyloid-beta and tau known to play key roles in Parkinson’s and Alzheimer’s disease, researchers report.

Caffeine, in contrast, had no effect on protein buildup in this early lab study, and researchers saw coffee consumption to offer no protection against alpha-synuclein aggregation.

The study, “Phenylindanes in Brewed Coffee Inhibit Amyloid-Beta and Tau Aggregation,” was published in Frontiers in Neuroscience.

Coffee consumption has been suggested to reduce the risk of developing diabetes, various cancers, and neurodegenerative disorders such as Parkinson’s and Alzheimer’s disease. Despite the available evidence, however, it’s unclear what how exactly coffee can help to prevent age-related cognitive decline.

Past studies have reported that caffeine, the main bioactive compound of coffee, can reduce the risk of Parkinson’s both in men and in women who were not taking hormone replacement therapy. It has also been seen to reduce nerve cell death in the substantia nigra – the brain area most affected in Parkinson’s – in mouse models of the disease.

However, recent data also suggests that long-term consumption of caffeine may exacerbate anxiety-related behavioral and psychological symptoms in patients with dementia, counteracting its potential beneficial effects.

These contrasting findings highlight the need to identify those coffee components that may be neuroprotective.

Researchers led by Donald Weaver, MD, PhD, co-director of the Krembil Brain Institute, evaluated the potential of chemical components of coffee to inhibit the buildup of proteins that can drive neurodegenerative diseases like Alzheimer’s and Parkinson’s, in particular: amyloid-beta, tau, and alpha-synuclein.

The team started by examining three types of instant coffees — light roast, dark roast, and decaffeinated dark roast — in terms of their ability to prevent protein aggregates. They tested the instant coffees by adding them to one of these three proteins in an in vitro (laboratory dish) context.

“The effect of caffeine content would be assessed by comparing the activity of caffeinated and decaffeinated dark roast coffee extracts. Further, since it is known that different levels of roasting affect the composition of the coffee brew, comparison of light versus dark roast coffee extracts was also performed,” the researchers wrote.

Dark roast coffee showed the greatest inhibitory effect against tau protein buildup. Interestingly, the level of caffeine in each type of coffee had no impact on tau, amyloid-beta, and alpha-synuclein’s ability to aggregate.

“We were surprised to find that caffeine content did not influence aggregation inhibition, and thus performed a post-hoc analysis of pure caffeine,” the researchers said in the study. “No effect on fibril growth was observed relative to the vehicle control, consistent with the results for caffeinated versus decaffeinated coffee extracts.”

Further experiments found that all coffee extracts could prevent amyloid-beta and tau protein aggregation at 200 μg/mL concentration. Dark roast coffee (with or without caffeine) was seen as more potent in preventing the oligomerization — a chemical form that proteins can take — of amyloid-beta than the light roast extract.

All types of coffee as an instant mix, however, showed an ability to promote alpha-synuclein aggregation at amounts above 100 mg/mL.

To better understand these findings, the team then explored the activity of the six main chemical components of coffee — caffeine, chlorogenic acid, quinic acid, caffeic acid, quercetin, and phenylindane.

Researchers found that most of these compounds — with exception of caffeine and quinic acid for amyloid-beta, and caffeine and caffeic acid for tau — prevented protein aggregation.

Phenylindane was found to hold the strongest inhibitory activity, working as a dual-inhibitor to prevent the formation of amyloid-beta aggregates by 99% and those of tau tangles by 95.2%. Importantly, in later experiments, phenylindanes did not show “pro-aggregation behavior” toward alpha-synuclein, the study reported.

Phenylindanes are formed during the roasting of coffee beans and are found in higher concentrations in dark roast coffees, which have longer roasting times.

“It’s the first time anybody’s investigated how phenylindanes interact with the proteins that are responsible for Alzheimer’s and Parkinson’s,” Ross Mancini, a research fellow in medicinal chemistry at the Krembil institute and the study’s first author, said in a news release.  “The next step would be to investigate how beneficial these compounds are, and whether they have the ability to enter the bloodstream, or cross the blood-brain barrier.”

The team is now investigating if phenylindanes can reduce amyloid-beta, tau and alpha-synuclein loads in cell and animal models of Alzheimer’s and Parkinson’s disease.

Researchers caution that their findings are not recommendation for excessive coffee consumption.

“What this study does is take the epidemiological evidence and try to refine it and to demonstrate that there are indeed components within coffee that are beneficial to warding off cognitive decline,” Weaver said. “It’s interesting, but are we suggesting that coffee is a cure? Absolutely not.”

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Blood Caffeine Levels May Help Diagnose Early Parkinson’s Disease, Study Reports

Caffeine as diagnostic tool

Parkinson’s patients have lower blood levels of caffeine and its byproducts after consuming the stimulant, suggesting that caffeine could be used as a biomarker for diagnosing the disease.

The findings appeared in the study “Serum caffeine and metabolites are reliable biomarkers of early Parkinson disease,” published in the journal Neurology.

Caffeine is an organic molecule that, when consumed through coffee or tea, can stimulate the central nervous system.

There is evidence that daily caffeine consumption reduces the risk of developing Parkinson’s both in men and in women who are not taking hormone replacement therapy.

In addition, caffeine and two of its metabolites — byproducts produced in the body —  reduce nerve cell death in the brain’s substantia nigra region, mice studies have shown. The substania nigra is the main brain area that Parkinson’s affects.

The researchers studied 108 Parkinson’s patients — 58 men and 50 women — and 31 healthy controls. The team also checked 67 other Parkinson’s patients — 33 men and 34 women — and 51 controls for mutations of caffeine-associated genes.

Participants drank between zero and five cups of coffee a day, except for one, who drank more than six.

Parkinson’s patients had lower blood serum levels of caffeine and nine of its metabolites — including the main byproducts theophylline, theobromine, and paraxanthine — than controls, researchers said. This was true regardless of the stage of patients’ disease and how much caffeine they were consuming.

Another finding was caffeine levels in patients with movement complications were lower than in those without.

Even though the findings showed a relation between caffeine serum levels and Parkinson’s, there was no significant association between the severity of the disease and the concentration of caffeine-related substances. There was also no significant difference in serum levels between men and women with Parkinson’s.

Importantly, researchers found no differences in caffeine-related gene mutations between patients and controls. They looked at genes involved in caffeine metabolism or that encoded the caffeine adenosine 2A receptor.

The results prompted the team to conclude that “caffeine metabolite profiles may be reliable diagnostic biomarkers for early Parkinson’s disease.”

Researchers acknowledged that the study had limitations. They noted that it “was conducted at a single university hospital” and that few participants had severe cases of Parkinson’s. The team excluded patients with a history of pneumonia or cancer.

In addition, any medications that participants were taking to deal with their Parkinson’s disease could have influenced their caffeine metabolism, the researchers said.

Nonetheless, the findings suggested that “lower levels of caffeine and caffeine metabolite profiles are promising diagnostic biomarkers” for early Parkinson’s disease, the team wrote.


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Source: Parkinson's News Today

Measuring Caffeine Levels in Blood Might Help Diagnose Early Parkinson’s, Study Suggests

blood caffeine levels

Low levels of blood caffeine and its metabolites may help identify patients with early Parkinson’s disease, according to new research. The findings are consistent with caffeine’s neuroprotective effects, previously observed in neurodegenerative diseases.

The study, “Serum caffeine and metabolites are reliable biomarkers of early Parkinson disease,” was published in the journal Neurology. The work was conducted by researchers at the Juntendo University School of Medicine in Tokyo, Japan.

A large number of epidemiological studies report a dose-responsive, inverse relationship between coffee/caffeine consumption and the risk of developing Parkinson’s. However, little is known about caffeine metabolism in Parkinson’s patients.

With that in mind, the team recruited 108 Parkinson’s patients without memory problems plus 31 age-matched healthy people as controls, and investigated their blood caffeine (and 11 of its metabolites) levels and whether there were mutations in their caffeine-related genes.

Both groups consumed the same amount of caffeine (about two cups of coffee a day).

Results showed that even early-onset Parkinson’s patients had significantly lower levels of caffeine and nine of its metabolites in their blood, compared to the control group. This was found to be unrelated to total caffeine intake or the severity of the disease.

“If these results can be confirmed, they would point to an easy test for early diagnosis of Parkinson’s, possibly even before symptoms are appearing. This is important because Parkinson’s disease is difficult to diagnose, especially at the early stages,” David G. Munoz, MD, of the University of Toronto in Canada, who wrote an editorial accompanying the study, said in a news release.

A statistical analysis revealed that this simple blood test was able to reliably identify Parkinson’s patients.

“Likewise, caffeine concentrations in patients with [Parkinson’s disease] with motor complications were significantly decreased compared with those without motor complications,” the team wrote.

When looking at the caffeine-associated genes, researchers reported no differences between Parkinson’s patients and healthy subjects.

Despite the promising results, this is a relative small study which needs to be replicated at a larger scale.

As part of the study’s limitations, people with severe Parkinson’s were not included, making it difficult to detect a relationship between disease severity and blood caffeine levels. Also, all Parkinson’s patients were medicated for the disease, which could influence caffeine metabolism, and thus the study results.

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Source: Parkinson's News Today