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Exposure to Second-Hand Smoke Linked to Lower Risk of Developing Parkinson’s, Study Suggests

second-hand smoke

Second-hand smoke may have a neuroprotective effect, as exposure to this type of indoor pollutant seems to be associated with a decreased risk of developing Parkinson’s disease, according to a recent study.

Conversely, exposure to certain air pollutants — like nitrogen dioxide and ozone — might contribute to a higher risk of developing the disease.

The study, “The impact of long-term exposure to ambient air pollution and second-hand smoke on the onset of Parkinson disease: a review and meta-analysis,” was published in Public Health.

Air pollution is composed of a variety of particulate air pollutants, volatile organic compounds, gaseous air pollutants, and airborne metals. Exposure to polluted air has been consistently associated with adverse effects in respiratory and cardiovascular diseases, but little is known about the effects of such exposure in neurodegenerative disorders such as Parkinson’s.

Although the exact causes behind Parkinson’s disease are not fully understood, it is thought to be induced by “a complicated interplay of environmental and genetic factors,” according to these researchers.

As such, “further investigation of the modifiable risk factors of [Parkinson’s disease] is of imperative significance and expected to have broad implication for the primordial prevention of this disease,” they said.

Second-hand smoke is a type of indoor air pollution. Evidence indicates that active smokers have a 50% lower chance of developing Parkinson’s in comparison with non-smokers. “However, whether this negative correlation is causal and persists among persons regularly exposed to SS [second-hand smoke] remains undetermined,” the researchers said.

To learn more, the scientists searched five medicine-related databases for any observational or epidemiological evidence on the relationship between long-term exposure to air pollution and second-hand smoke and Parkinson’s susceptibility.

The studied air pollutants included: particulate matter with an aerodynamic diameter of less than 2.5 μm (PM2.5), such as combustion particles, organic compounds, and metals; particulate matter with less 10 μm in diameter (PM10), including dust, pollen, and mold; nitrogen dioxides (NO2); ozone (O3); and carbon monoxide.

The researchers combined the results of 21 studies, involving a total 222,051 Parkinson’s patients, and performed a statistical review known as a meta-analysis.

A marginally significant higher risk of developing Parkinson’s disease was observed in those exposed to PM2.5, NO2, and O3. Although carbon monoxide was found to be positively associated with Parkinson’s susceptibility, statistical significance was not attained.

“Second-hand smoke conferred reduced risk of Parkinson disease, regardless of exposure occasions [at home/at work/in children] and timing,” the researchers said. This suggests that second-hand smoke might have a neuroprotective effect in those who are susceptible to developing Parkinson’s at some point in their lives.

Some possible explanations exist as to why cigarette smoke may be associated with a lower risk of Parkinson’s. One theory is that some tobacco smoke compounds contain properties that inhibit monoamine oxidase (MAO), an enzyme that plays a key role in the activation of MPTP, a well-known Parkinson’s-inducing neurotoxin, and that is involved in the degradation process of dopamine released by nerve cells.

“Other hypotheses include the direct neuroprotective effect of nicotine by stimulating dopamine release, upregulating nicotinic receptors, and inhibiting alpha-synuclein fibrillation, thereby suppressing and relieving parkinsonian symptoms,” the researchers said.

Given the many harmful effects of air pollutants, public and environmental health strategies that reduce outdoor air pollution levels could help lower the burden of Parkinson’s disease.

Despite the potential neuroprotective effect of second-hand smoke, caution is advised when interpreting these results, as more large-scale studies are necessary to fully understand such an association.

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People With Bipolar Disorder Face Higher Risk of Later Developing Parkinson’s, Study Finds

bipolar disorder

People with bipolar disorder have a significantly increased risk — more than three times that of the general population — of later developing Parkinson’s disease, a study has found.

Although use of medications for bipolar disorder could overestimate this risk, the researchers believe that a Parkinson’s diagnosis should be considered if patients with the mental health condition also show parkinsonian features.

The study, “Risk of Developing Parkinson Disease in Bipolar Disorder – A Systematic Review and Meta-analysis,” was published in JAMA Neurology.

Biopolar disorder is a mood disorder characterized by cyclic episodes of depression and mania. Although the mechanisms underlying bipolar disorder are still not completely understood, there is a possible role of the dopaminergic system — which is affected in Parkinson’s disease.

In fact, antipsychotic medications that block dopamine receptors can improve manic symptoms in these patients.

Certain medications used to treat bipolar disorder — such as lithium, antipsychotic medications, and antiepileptic medications — could be associated with drug-induced parkinsonism, which cannot be effectively distinguished from Parkinson’s disease in the clinic.

“Since drug-induced parkinsonism is more common among patients with [bipolar disorder], physicians may be more inclined to misdiagnose PD as drug-induced parkinsonism,” the researchers said.

Some studies also have shown that bipolar disorder is more common in people with Parkinson’s.

To understand the possible association of bipolar disorder with a later diagnosis of idiopathic Parkinson’s disease — meaning it’s due to an unknown cause — researchers from the University of Lisbon in Portugal performed an electronic literature search across four medicine-related databases.

Data from seven studies, involving 4, 374, 211 total participants, were used. The selected studies contained data on the likelihood of developing Parkinson’s disease in individuals with bipolar disorder versus those who did not have this condition.

The results showed that those with bipolar disorder were 3.4 times more likely to develop Parkinson’s disease later in life. Even when accounting for studies that had a high risk of bias, this likelihood was still maintained, albeit lower, at 3.21 times greater risk.

Researchers then performed a subgroup analysis in which they divided participants based on the duration of their follow-up. Specifically, they split patients into two groups: one including participants with more than nine years of follow-up versus those who were followed for less time.

Both groups had an increased risk of developing Parkinson’s, but the subgroup with the shorter follow-up was associated with a greater increase in the risk of a PD diagnosis.

However, this could be due to a higher rate of misinterpretation of drug-induced parkinsonism as Parkinson’s disease. “In fact, one study explicitly did not differentiate between the 2 conditions,” the researchers said.

“This review suggests that patients with [bipolar disorder] have a significantly increased risk of developing PD compared with the general population,” the researchers said.

They added that, if patients with bipolar disorder show parkinsonism features, a Parkinson’s diagnosis should be considered “independently of concomitant medication.”

The investigators said further testing could help to determine whether patients presented Parkinson’s versus drug-induced parkinsonism.

“To clinically distinguish parkinsonism from PD in clinical practice, the use of functional neuroimaging methods may be of particular interest,” they said.

“The main clinical implication of this review should be to underline that if patients with [bipolar disorder] present with parkinsonism features, this may not be drug induced and may recommend the investigation of PD,” the researchers concluded.

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Specific Parkinson’s Gene Mutation Linked to Higher Risk of Leukemia, Colon Cancer, Study Finds

gene mutation cancer risk

People with Parkinson’s disease who have a specific mutation in the LRRK2 gene may be 10 times more likely to develop leukemia, and twice as likely to have colon cancer, researchers report.

The researchers say this particular patient population should be closely monitored and screened for the early detection of cancer.

These findings, “Cancer Outcomes Among Parkinson’s Disease Patients with Leucine Rich Repeat Kinase 2 Mutations, Idiopathic Parkinson’s Disease Patients, and Nonaffected Controls,” were published in Movement Disorders.

Mutations in the leucine rich repeat kinase 2 (LRRK2) gene are one of the most commonly known genetic causes of Parkinson’s disease. They usually result in the malfunctioning of lysosomes — special compartments within cells that digest and recycle different types of molecules. Lysosomal dysfunction is involved in the formation of Lewy body protein aggregates and, therefore, neurodegeneration.

Different studies indicate Parkinson’s patients with a specific mutation in the LRRK2 gene, known as G2019S, have an increased risk of developing certain cancers compared with people with Parkinson’s disease of unknown cause.

“However, it is unclear whether the increased risk among LRRK2-PD [Parkinson’s disease] patients would be observed when compared with unaffected controls who are noncarriers of the G2019S mutation,” the researchers said.

Investigators from the Albert Einstein College of Medicine and Mount Sinai Beth Israel Medical Center sought to compare the prevalence of cancer among Parkinson’s patients with the LRRK2 mutation, people with Parkinson’s of unknown cause (also called idiopathic Parkinson’s), and healthy individuals (controls). To do so, they used a standardized questionnaire across seven international LRRK2 and Parkinson’s-related research centers.

The gathered data was then combined with previously published information to examine the associations between the LRRK2 G2019S mutation and several types of cancer.

Researchers studied the cancer outcomes of 257 LRRK2 G2019S Parkinson’s patients, 712 people with idiopathic Parkinson’s, and 218 genetically unrelated controls, ages 35 or older. On average, the Parkinson’s patients were 68.2 years old, while the control sample was 4 years younger, with a mean age of 64 years. Around 77% of study subjects were Ashkenazi Jews, who more commonly carry genetic mutations linked to Parkinson’s, such as LRRK2.

Results showed there were no significant differences in the cancer rates of all three study groups. In fact, the rates were similar: 32.3% for LRRK2 G2019S Parkinson’s patients, 27.5% for idiopathic Parkinson’s, and 27.5% for controls.

Nevertheless, individuals with the LRRK2 G2019S mutation had a 4.6-fold increased risk of developing leukemia, and a 1.6-fold higher risk of developing skin cancer. Researchers note that only 5 of the 257 people with LRRK2 G2019S Parkinson’s developed leukemia, compared with no cases in the idiopathic Parkinson’s group. Further analysis also suggested higher risks for colon and kidney cancers in LRRK2 G2019S Parkinson’s, but statistical significance was not attained.

Scientists then combined this data with that of a previous study, which led to an overall study pool totaling 401 people with LRRK2 G2019S Parkinson’s and 1,946 individuals with the idiopathic form of the neurodegenerative disorder.

The pooled analysis revealed that individuals with LRRK2 G2019S were 9.84 times more likely to develop leukemia, and 2.34 times more likely to develop colon cancer, in comparison with idiopathic Parkinson’s patients.

These findings indicate the LRRK2 G2019 mutation might be associated with the development of several types of cancer.

“We might consider that if someone is a carrier of the LRRK2 G2019S mutation they should be closely monitored for Parkinson’s and for certain cancers,” Ilir Agalliu, MD, PhD, associate professor in the department of epidemiology and population health at Albert Einstein College of Medicine, and first author of the study, said in a press release.

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High Corticosterone Levels a Risk Factor for Parkinson’s, Mouse Study Finds

corticosterone mouse study

High levels of corticosterone — a hormone that regulates energy, immune, and stress responses — is a risk factor for the development and progression of Parkinson’s disease, according to a mouse study.

The study, “Chronic corticosterone aggravates behavioural and neuronal symptomatology in a mouse model of alpha-synuclein pathology,” was published in the journal Neurobiology of Aging.

Parkinson’s disease is a neurodegenerative disorder mainly resulting from the gradual loss of dopaminergic neurons in the substantia nigra, a region of the brain responsible for controlling body movements.

This is a consequence of overproduction and misfolding of the protein alpha-synuclein in neurons, which leads to the formation of small toxic deposits called Lewy bodies that gradually damage and kill nerve cells. Growing evidence has demonstrated that these alpha-synuclein aggregates are associated with Parkinson’s onset and progression.

“Injection of alpha-synuclein preformed fibrils (PFFs) in different brain regions … induces pronounced alpha-synuclein pathology [aggregate] propagation. Interestingly, in these [mouse] models the amygdala is among the brain regions most severely affected by alpha-synuclein pathology [disease],” the researchers wrote.

The amygdala is an area of the brain involved in memory, decision-making, and emotional responses. Several non-motor symptoms in Parkinson’s, including anxiety and depression, have been linked to structural alterations and functional impairments of the amygdala.

“Similarly, chronic stress and glucocorticoid [imbalance] change amygdala physiology [function], and indeed are involved in the development of anxiety and depression,” they wrote.

The group of researchers from the Brain Mind Institute at the École Polytechnique Fédérale de Lausanne in Switzerland set out to investigate if mood/emotional alterations linked to amygdala dysfunction might accelerate the formation and propagation of alpha-synuclein aggregates associated with Parkinson’s in a mouse model of the disease.

To test their hypothesis, they first treated mice with corticosterone, a glucocorticoid that is normally produced in response to stress, to mimic the effects of depression and chronic stress in the amygdala.

Animals were then injected on one side of the brain’s striatum — a region involved in motor and cognitive control — with either alpha-synuclein preformed fibrils to trigger the formation and propagation of alpha-synuclein aggregates across the whole brain, or with a saline solution (vehicle control).

Chronic treatment with corticosterone triggered depression in animals and had a strong effect on their body shape, fat deposition, body weight, and drinking and eating habits. Injection of alpha-synuclein preformed fibrils had no effects on any of these parameters.

Behavioral tests performed one to two months after the injection of alpha-synuclein showed that animals that had been injected with these fibrils displayed mild anxiety, which was reversed by corticosterone treatment.

However, they found that chronic treatment with corticosterone in animals that had been injected with preformed fibrils led to the accumulation of phosphorylated alpha-synuclein in specific regions of the brain, including the entorhinal cortex, a region involved in memory, spatial navigation, and time perception.

Alpha-synuclein phosphorylation is a chemical modification in which a phosphate group is added to the protein. It 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 aggregates.

They also discovered that treatment with corticosterone in mice that had been injected with alpha-synuclein fibrils increased the loss of dopaminergic neurons.

“We report aggravated alpha-synuclein pathology [disease] and neurodegeneration in mice injected with alpha-synuclein [preformed fibrils] in a condition of heightened corticosterone, suggesting heightened glucocorticoid levels as a risk factor for the development of the neuropathological hallmarks of Parkinson’s disease and potential target for treatment,” the researchers wrote.

“Further studies aimed at elucidating the vulnerability factors of specific brain regions to alpha-synuclein pathology, and why at some point resilience fails and neurodegeneration (such as in the substantia nigra) occurs, are needed and will greatly enhance our understanding of the role of alpha-synuclein pathology in the [development] of Parkinson’s disease and synucleinopathies,” they added.

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Brain Serotonin Changes May Be Early Warning Sign of Parkinson’s, Study Suggests

serotonin early warning

Changes to the serotonin system in the brain occur years before the development of motor symptoms in Parkinson’s — and may be an important early warning signal for the disease, a study suggests.

“Therefore, brain imaging of the serotonin system could become a valuable tool to detect individuals at risk for Parkinson’s disease, monitor their progression and help with the development of new treatments,” Heather Wilson, research associate at King’s College London and the study’s first author, said in a press release.

The study, “Serotonergic pathology and disease burden in the premotor and motor phase of A53T α-synuclein parkinsonism: a cross-sectional study,” was published in The Lancet Neurology.

Parkinson’s is characterized by the progressive death of brain cells that are responsible for producing dopamine, which eventually leads to the development of motor symptoms associated with the disease, including involuntary tremors or muscle contraction.

Studies have suggested that, in addition to changes in the dopaminergic system, Parkinson’s progression and symptoms may be associated with impaired signals from another important neurotransmitter, called serotonin. Serotonin transmits messages between nerve cells, and is thought to be active in constricting smooth muscles.

To further explore the role of serotonin in Parkinson’s progression, a team led by researchers from King’s College evaluated non-symptomatic carriers of an alpha-synuclein (SNCA) gene variant. That variant is an extremely rare mutation, but a well-known cause for hereditary Parkinson’s disease.

Individuals with mutations in the alpha-synuclein gene are almost certain to develop Parkinson’s during their lifetime, which makes them invaluable candidates to study the biological events that result in the development of the disease.

The study recruited 14 individuals who were carriers of the A53T variant in the SNCA gene, as well as 25 patients with idiopathic (of unknown cause) Parkinson’s disease, and 25 healthy matched volunteers who had no history of neurological or psychiatric disorders.

All participants were evaluated by positron emission tomography (PET) scans. PET scans use a specific dye that binds to the serotonin transporter, and evaluates serotonin metabolism in the brain. Participants also underwent several clinical assessments to determine motor and non-motor symptoms. They were evaluated for cognitive status, dopamine metabolism, and brain structural changes.

Among individuals who were SNCA mutation carriers, 50% were still asymptomatic —  at the premotor stage of the disease — and had dopaminergic deficits.

Compared with healthy controls, the premotor SNCA carriers showed reduced serotonin signals in several brain areas. SNCA carriers who still had normal dopamine transporters already showed “an average of 34% loss of serotonin transporters in raphe nuclei and 22% loss in the striatum compared with healthy controls,” the researchers said.

As the name indicates, a serotonin transporter is a protein that binds to and transports serotonin to different areas of the brain. Raphe nuclei are a type of brain receptor that decrease the release of serotonin. The striatum is a critical brain region involved in voluntary movement.

“Parkinson’s disease has traditionally been thought of as occurring due to damage in the dopamine system, but we show that changes to the serotonin system come first, occurring many years before patients begin to show symptoms,” said Marios Politis, MD, PhD, professor at the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) and senior author of the study.

Those who were SNCA carriers but had already been diagnosed with Parkinson’s disease showed more extensive deficits in the serotonin system, affecting even more areas of the brain. There was 48% serotonin transporter loss in the raphe nuclei, and 57%  loss in the striatum areas.

Further analysis revealed that low serotonin signals in the brainstem were associated with increased total scores on the Movement Disorder Score-Unified Parkinson’s Disease Rating Scale (MDS-UPSRS) — indicating higher disease burden. This occurred in all SNCA carriers, and in those with idiopathic Parkinson’s.

“Our findings provide evidence that molecular imaging of serotonin transporters could be used to visualize premotor pathology of Parkinson’s disease in vivo [in the body],” the researchers said.

Future studies should focus on implementing serotonin transporter imaging as “an adjunctive tool for screening and monitoring progression” for those at risk for, or who already have Parkinson’s.

“This is one of the first studies to suggest that changes in serotonin signaling may be an early consequence of Parkinson’s,” said Beckie Port, PhD, research manager at Parkinson’s UK. “Picking up on the condition earlier and being able to monitor its progression would aid the discovery of new and better treatments that could slow the loss of brain cells in Parkinson’s.”

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Specific BDNF Mutation May Be Linked to Higher Risk of Cognitive Impairment in Parkinson’s, Study Suggests

BDNF gene mutation

One amino acid change in the brain-derived neurotrophic factor (BDNF) gene, which provides instructions for a protein important to neuronal survival, may be associated with cognitive impairment in Parkinson’s disease patients, a study has found.

The study, “BDNF Val66Met polymorphism and cognitive impairment in Parkinson’s disease—a meta-analysis,” was published in the journal Neurological Sciences.

BDNF protein is produced inside brain cells and is crucial for their function as well as supporting their growth and protecting them against premature cell death. When its coding sequence is changed, this can have a major impact on brain cell outcomes.

Previous studies have suggested that one specific BDNF gene mutation called Val66Met that results in the change of a valine (Val) by a methionine (Met) at position 66 — both amino acids, also known as the protein’s building blocks — could be linked to cognitive impairment in Parkinson’s disease. However, there is no consensus on the relevance of this genetic mutation on outcomes of Parkinson’s patients.

Chinese researchers searched for available literature on this matter, and analyzed pooled data from six studies involving a total of 1,467 patients with Parkinson’s disease. These studies had been carried out in Italy, Spain, Poland, Brazil, Belgrade (Serbia), and the Netherlands.

Results revealed a significant association between the Val66Met BDNF mutation and risk of Parkinson’s disease-related cognitive impairment. Patients who had two copies of the BDNF gene with methionine (mutated version) were found to have a 3.82 times higher risk of developing cognitive impairment than those who had two BDNF copies with valine (non-mutated version).

However, it’s worth mentioning that the studies in this analysis only included Caucasian study samples, so these results should not be generalized to other ethnicities.

Parkinson’s disease affects people of all races and ethnicity worldwide. Some studies indicate that neurodegenerative disorders affect more white people than any other ethnicity, but a solid conclusion cannot be drawn from available research as they tend to vary widely regarding diagnostic criteria, sample sizes, and methodology.

“Future studies should verify our findings in larger populations, particularly in other ethnicities,” the researchers wrote.

Still, the team believes that this study provides evidence that mutated BDNF “may be associated with increased risk of cognitive impairment of Parkinson’s disease, at least among Caucasians.”

In addition, this Val66Met change in the BDNF sequence should be studied in different Parkinson’s patients presenting tremor dominant or postural instability gait disorders. Further understanding of the impact of genetics on the long-term outcomes of these patients “may better guide clinical treatments and judge the prognosis,” they said.

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Low Levels of Substance P in Saliva May Help Predict Swallowing Problems, Study Suggests

substance P dysphagia

Low levels in saliva of a molecule called substance P may help predict the development of swallowing problems in people with Parkinson’s disease, a small pilot study in Germany found.

Since this molecule works as communication signal between nerve cells in the body, this discovery suggests that impaired substance P activity may be an important contributing factor in the  development of this Parkinson’s complication.

The study, “Substance P Saliva Reduction Predicts Pharyngeal Dysphagia in Parkinson’s Disease,” was published in the journal Frontiers in Neurology.

The progression of Parkinson’s disease is associated with the loss of movement control, including control over muscles in the face, mouth, and throat. This can lead to speech problems and swallowing difficulties, which are known medically as dysphagia.

Such swallowing difficulties can severely affect a person’s ability to sustain healthy eating practices without needing additional support.

“Parkinson’s-related dysphagia affects the oral, pharyngeal and the esophageal phase of swallowing and occurs in all stages of the disease,” the researchers said.

However, this complication may remain undetected during early stages of Parkinson’s in many patients, which may prevent early diagnosis and timely care, they said.

Previous studies have shown that levels of the neurotransmitter substance P are reduced among elderly Parkinson’s patients who have aspiration pneumonia. This suggests that substance P may be involved in the underlying mechanism of the normal swallowing and cough reflex in the throat’s inner tissues, called the pharyngeal mucosa.

To learn more, German researchers explored the role of substance P in the progression of pharyngeal dysphagia in people with Parkinson’s.

The study enrolled 20 patients; half showed signs of swallowing difficulties. Researchers collected saliva samples from all patients and analyzed the levels of substance P.

Participants who did not have pharyngeal dysphagia were slightly younger, had Parkinson’s for fewer years, and also showed fewer signs of motor impairments caused by the disease as compared to patients with the complication. However, these differences were minor, and the groups were considered to be at similar disease stages.

The results showed that patients who did not have swallowing problems had 1.8-fold higher levels of substance P than those with dysphagia.

“Our findings could be another indication that, in early stages, loss of substance P containing neurons in the pharyngeal mucosa may lead to pharyngeal hyposensitivity and merely incipient pharyngeal dysphagia,” the researchers said.

Additional studies are warranted to further understand the role of substance P in Parkinson’s disease progression, the researchers said. They also recommended that further studies be done to evaluate substance P’s potential as a biomarker for early dysphagia.

Future research also should address the potential use of capsaicin — an active compound in chili peppers known to stimulate the release of substance P — as strategy to target the sensory system within the swallowing network of nerve cells, they added.

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High Levels of Inflammatory Biomarker Evident in Patients, Study Says, But Cause-Effect Unknown

c-reactive protein inflammation

Parkinson’s disease patients have “significantly elevated” levels of c-reactive protein, an acute-phase biomarker for inflammation in the body, according to a recent literature review.

It remains to be understood, however, if c-reactive protein is a risk factor for this neurodegenerative disorder, or if the disease itself triggers an inflammatory response.

The study, “C-reactive Protein and Risk of Parkinson’s Disease: A Systematic Review and Meta-analysis” was published in Frontiers in Neurology.

Chronic neuroinflammation is a hallmark of Parkinson’s disease (PD). Studies have suggested that inflammatory processes may contribute to disease risk and progression, although this biological response is unlikely to be the primary cause of neuronal death.

Evidence indicates that high c-reactive protein (CRP) levels are strongly correlated with the inflammatory process. Indeed, some studies suggest a link between CRP and chronic inflammatory and neurodegenerative disorders, such as cardiovascular disease, Alzheimer’s disease, or Parkinson’s.

Although some population-based studies have explored the relationship between c-reactive protein levels and Parkinson’s risk, results so far have been contradictory.

That led researchers at the First Affiliated Hospital of Guangxi Medical University, in China, to analyze all available studies regarding c-reactive protein levels in the serum, plasma, blood, and cerebrospinal fluid — the liquid that surrounds the brain and spinal cord — in Parkinson’s patients.

Investigators searched the records of seven life sciences, biomedical or medical databases — three of them Chinese — up through October 2018, examining associations between c-reactive protein levels and Parkinson’s risk.

The team analyzed a total of 23 case-control studies published between 2009 and 2018, which involved 2,646 Parkinson’s patients (mean age 63.6–73.2) and 1,932 controls. Disease duration ranged from 3 months to 9.8 years.

Whether studies used standard or more sensitive immunoassays — a procedure used to measure certain immune-related proteins or substances — c-reactive protein concentration in whole blood, serum, and cerebrospinal fluid was found to be significantly, and consistently, higher in Parkinson’s patients than in healthy controls.

Other factors, such as the patient’s medication use or other accompanying diseases, also may affect c-reactive protein levels, the researchers said.

Although the findings indicate a link between c-reactive protein levels and Parkinson’s, it is still unknown whether this “measurable” biochemical inflammation contributes to, or is a consequence of, Parkinson’s-related neurodegenerative mechanisms.

“[T]here is growing evidence that support an association between neuroinflammation and the initiation and progression of PD pathophysiology,” the researchers wrote.

“The results of this review only suggested a correlation between CRP levels and PD, but could not completely delineate whether inflammation plays a causal role in PD, or if PD leads to inflammatory processes,” they concluded.

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Having a Heart, Lung, Kidney, or Bone-Marrow Transplant May Lower Risk of Developing Parkinson’s

transplant

People who have had kidney, heart, lung, or bone-marrow transplants are less likely to develop Parkinson’s disease than the general population, research suggests.

The study, “Transplant and risk of Parkinson disease” was published recently in Parkinsonism & Related Disorders

Chronic neuroinflammation is a hallmark of Parkinson’s disease with studies suggesting that inflammatory processes contribute to disease risk and progression, although such biological response is unlikely to be the primary cause of neuronal death. That is why researchers suspect that reducing inflammation in the brain has the potential to slow neurodegeneration.

Anti-rejection drugs, also known as immunosuppressant medications, inhibit the immune system’s activity and reduce overall inflammation in the body, including the central nervous system.

Patients who undergo organ transplants usually are given these types of medicines to lower their body’s ability to reject the transplanted organ.

“Because inflammation may play a role in the pathophysiology of PD [Parkinson’s disease], it is possible that immunosuppressants could reduce the risk” of the disease, researchers wrote.

A team led by Washington University School of Medicine in St. Louis researchers investigated the risk of Parkinson’s disease in relation to tissue transplant. This same team had shown previously that individuals taking selected immunosuppressants had a lower risk of Parkinson’s disease than the general population Medicare beneficiaries who were studied.

In the most recent study they assessed Medicare beneficiaries (age 66–90 years) data from 2004 to 2009 and identified 89,790 Parkinson’s disease cases. For the control group, researchers selected a 0.5% random sample of all Medicare beneficiaries included in the study period, totaling 118,095 subjects.

History of kidney, heart, lung, bone-marrow, pancreas or cornea transplant was then registered. There were 278 transplants in the Parkinson’s sample and 302 in the control group.

Statistical analysis revealed patients who underwent transplants had a 37% lower risk of developing Parkinson’s than the general Medicare population.

“Overall, patients who had undergone tissue transplant more than five years prior to PD [Parkinson’s disease] diagnosis or reference had lower risk of PD,” researchers wrote.

This correlation was consistent for kidney, heart, lung, and bone-marrow transplants. Liver or corneal (the transparent layer that makes up the front of the eye) transplant was not linked to Parkinson’s disease risk.

When adjusting for underlying cause of the transplants, such as valvular heart disease, diabetes with renal complications, or chronic hepatitis infection, organ transplant remained inversely correlated with Parkinson’s risk. However, the association with kidney transplant became statistically non-significant.

“This study provides evidence that tissue transplant may be associated with a lower PD [Parkinson’s disease] risk, warranting further investigation to identify factors that mediate this relationship, including a potential effect of immunosuppressive therapy on PD risk,” researchers concluded.

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Subjective Cognitive Decline Could Help Predict Parkinson’s Dementia, Study Contends

cognitive decline

Subjective cognitive decline in Parkinson’s disease could predict the development of dementia. As such, a suitable cognitive screening test could help provide an accurate diagnosis and prognosis.

The study with those findings, “Subjective cognitive decline and progression to dementia in Parkinson’s disease: a long-term follow-up study,” was published in Journal of Neurology.

Even during the early stages of disease, mild cognitive impairment can affect non-demented Parkinson’s patients, and is considered a risk factor for the development of dementia (PDD).

In fact, the prevalence of PDD increases as the disease progresses: from 28% after five years of evolution to 80% after 20 years of the disease.

Subjective cognitive decline — self-reported acquired difficulties with cognitive functioning — is common in the elderly and can be used as a predictor of dementia. In Alzheimer’s disease, subjective cognitive decline has been linked to disease-related tissue/molecular changes and a higher risk for dementia development. However, the predictive value of this type of cognitive status impairment has not been demonstrated yet in Parkinson’s disease.

Scientists from the University of La Laguna, Spain, investigated the neuropsychological profile of subjective cognitive decline in Parkinson’s disease and explored which components could better predict the development of PDD. The team also compared different screening tests to assess subjective cognitive complaints.

A total of 43 Parkinson’s patients and 20 healthy subjects were subjected to neuropsychological examination using a battery of cognitive tests. All patients were being medicated for Parkinson’s and were evaluated during their “on” state — when they are responding to medication and have reduced symptoms.

Subjective cognitive decline was diagnosed using two distinct approaches. A semi-structured interview in which the patient provided his/her subjective opinion on his/her attention, memory, spoken language, naming, written language, visuospatial skills and executive functions; diagnosis was considered when the patient had at least one cognitive complaint. Additionally, a subjective cognitive decline diagnosis also was established on the basis of the interview question concerning memory complaint.

For a mild cognitive impairment diagnosis, investigators followed the criteria proposed by the Movement Disorder Society (MDS)

Based on the results of the interview and on the MDS Task Force criteria, patients were diagnosed as having either subjective cognitive decline or mild cognitive impairment. Of the 43 patients, 13 (30.2%) were diagnosed with subjective cognitive decline, 22 (51.2%) with mild cognitive impairment and 8 (18.6%) had no subjective cognitive complaints. Difficulties in naming and memory were the most frequent cognitive complaints.

Based on memory complaints alone 10 patients (23.25%) were diagnosed with subjective cognitive decline. Interestingly, 10 of the 22 (45.45%) who had been diagnosed with mild cognitive impairment reported no memory complaints.

Mild cognitive impairment subjects performed poorer in the processing speed (the time it takes a person to do a mental task), executive functions (a set of mental skills that helps with organization and regulation), visuospatial skills, memory, and language domains, compared to the other groups.

There were no significant differences between healthy participants (controls)  and Parkinson’s disease patients with subjective cognitive decline in any of the neuropsychological measures.

The team also assessed how many patients diagnosed with subjective cognitive decline progressed to dementia after a mean follow-up of 7.5 years. Fifty percent of mild cognitive impairment patients, 33.3% of individuals diagnosed with subjective cognitive decline, and 14.3% of patients without subjective cognitive complaints developed dementia, which was found to be associated with a poor performance in verbal and visuospatial memory and naming at the beginning of the study.

Additionally, both the language and memory domains were good predictors of dementia development.

“These results are highly relevant for future investigations and also for clinicians: the [subjective cognitive decline] assessment is frequently the first step of cognitive examination and can influence future decisions (e.g., to administer a screening test or a comprehensive neuropsychological assessment),” researchers wrote.

“Assessments that do not include procedures to adequately explore cognitive complaints may underestimate the proportion of [Parkinson’s-related subjective cognitive decline] and, therefore, [mild cognitive impairment] and thus misclassify patients as [Parkinson’s disease] with normal cognition, especially when brief cognitive examinations are chosen,” they concluded.

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