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Patients with Bipolar Disorder at Higher Risk of Developing Parkinson’s, Study Suggests

bipolar disorder

Patients with bipolar disorder appear to have a nearly seven times higher risk of developing Parkinson’s disease later in life, according to a nationwide study in Taiwan.

The study, “Bipolar disorder and risk of Parkinson disease: A nationwide longitudinal study,” was published in the journal Neurology.

An association between major depressive disorder and Parkinson’s disease has been suggested in previous studies. But such an analysis has not been conducted in people with bipolar disorder, which is characterized by unusual shifts in mood, energy, and activity levels.

Data from a hospital registry previously showed that people with manic or depressive episodes — both experienced by those with bipolar disorder — had an increased risk of being diagnosed with Parkinson’s, but the temporal link between these two events had not yet been properly assessed.

To address this lack of knowledge, researchers conducted a longitudinal study using Taiwan’s National Health Insurance Research Database. Clinical records from 56,340 patients with bipolar disorder (mean age 40 years) and 225,360 healthy individuals, collected between 2001 and 2009 and followed until 2011, were evaluated. None of the participants had a history of Parkinson’s or related diseases at the start of the study.

Patients with bipolar disorder developed Parkinson’s significantly more often than those in the control group (0.7% vs, 0.1%). These patients also had a shorter time from enrollment to Parkinson’s disease diagnosis (4.2 vs. 6.5 years), and were younger when Parkinson’s was identified (64.2 vs. 73 years).

Use of antipsychotic agents was found to have no impact on these findings. The prevalence of cerebrovascular diseases, traumatic brain injury, hypertension, dyslipidemia (abnormal levels of lipids), and diabetes did not differ between the two groups.

Further analysis revealed that adult bipolar patients were about 6.78 times more likely to develop Parkinson’s than controls, while bipolar patients older than 65 had a 3.87 times higher risk.

Patients with a high frequency of hospital admission (more than two times per year) for psychiatric episodes were found to have 5.62 times higher risk of Parkinson’s than patients admitted less than once a year. Also, two or more psychiatric admissions for manic/mixed or depressive episodes were associated with a greater likelihood of having Parkinson’s.

“Our population-based longitudinal study found that patients with bipolar disease had an increased risk of developing [Parkinson’s] later in life compared to the controls,” the researchers wrote.

“Additional experiments are required to obtain a deeper understanding of the mechanisms involved” in the development of these two disorders,” they said. In addition, “medical practitioners should be aware that the risk of subsequent [Parkinson’s] should be particularly considered in patients with bipolar disease, especially those with multiple psychiatric admissions for mood episodes.”

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Exposure to Air Pollution Not Linked to Parkinson’s, Study Suggests

air pollution risk

Long-term exposure to outdoor air pollution does not directly contribute to the development of Parkinson’s disease later in life, results from a Dutch study suggest.

Still, non-smoking women and people with long-term residential stability were found to be at greater risk of developing the disease, according to the study.

The study, “Parkinson’s disease and long-term exposure to outdoor air pollution: A matched case-control study in the Netherlands,” was published in the journal Environment International.

The cause of Parkinson’s disease remains largely unknown, though researchers suspect a combination of environmental and genetic factors. Despite efforts to uncover possible risk factors and contributors for Parkinson’s development and progression, the available data are still controversial. Studies have demonstrated that exposure to pesticides is a risk factor; in contrast, exposure to cigarette smoke can be protective.

Ambient air pollution has also been suggested as a potential risk factor for the development of Parkinson’s through various biological processes. However, studies performed on this topic have so far been inconsistent in their findings.

Therefore, a group of researchers from the Netherlands and Chile conducted a study to better understand the association between long-term exposure to ambient air pollution particles and the development of Parkinson’s disease.

Exposure to air pollution, which was defined as exposure to particulate matter with an aerodynamic diameter of less than 10 μm [PM10], less than 2.5 μm [PM2.5], between 2.5 μm and 10 μm [PMcoarse], black carbon, and nitrogen oxides [NO2 and NOx], were predicted based on a statistical model developed within the European Study for Air Pollution Effects (ESCAPE) study.

A total of 1,290 subjects, 436 of whom were Parkinson’s patients and 854 without progressive neurological disorders, were recruited from five hospitals in four cities in the Netherlands, and 16 years of air pollution exposure were estimated.

In general, the team did not find any significant relationship between exposure to ambient air pollutants and Parkinson’s disease, regardless of the type of pollutant.

The risk of developing Parkinson’s disease was found to be similar between individuals who had been more exposed to air pollutants and those who had been less exposed. In fact, the team reported a trend for a protective effect, with people more exposed having a slightly reduced risk. But these differences were not found to be statistically relevant.

“We found no clear association between 16 years of residential exposure to ambient air pollution and the development of Parkinson’s disease in The Netherlands,” researchers said.

Still, in additional analysis the team found evidence that non-smoking women and those who lived for at least 14 years at the same residence were at higher risk of developing Parkinson’s disease with increased exposure to ambient air pollution. However, given the limited number of participants, further studies are required to validate these subgroup findings.

“Additional work, considering longer exposure times, may assist in further understanding what (if any) role ambient air pollution plays in the risk of developing Parkinson’s disease,” researchers concluded.

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Appendectomy Is Linked to Higher Risk of Parkinson’s, Study Suggests

appendix

People who have appendectomies have more than three times the risk of developing Parkinson’s disease, according to the findings of a U.S. large-scale study.

The study, “Parkinson’s Disease Is More Prevalent In Patients With Appendectomies: A National Population-Based Study,” will be presented during Digestive Disease Week (DDW) 2019, May 18-21 in San Diego, California.

One of the hallmark features of Parkinson’s disease is the accumulation of toxic aggregates of alpha-synuclein protein that can result in the degeneration of nerve cells.

These aggregates, also known as Lewy bodies, are commonly detected in brain cells of Parkinson’s patients, causing the well-known motor symptoms associated with the disease, such as tremors and balance problems. But these protein clumps can also accumulate in the cells that innervate the gastrointestinal (GI) tract early on in the onset of Parkinson’s disease.

This evidence has suggested that the GI tract could play a role in development of the disease.

“Recent research into the cause of Parkinson’s has centered around alpha-synuclein, a protein found in the gastrointestinal tract early in the onset of Parkinson’s,” Mohammed Z. Sheriff, MD, lead author of the study and a physician at Case Western Reserve University and University Hospitals Cleveland Medical Center, said in a press release. “This is why scientists around the world have been looking into the gastrointestinal tract, including the appendix, for evidence about the development of Parkinson’s.”

Results from previous studies have suggested that appendectomies, a surgery in which the appendix is removed, could increase the risk of having Parkinson’s disease. However, data on this topic have been conflicting.

To shed light on this matter, researchers reviewed clinical records stored by Explorys, a commercial database that contains electronic health records from 26 major integrated U.S. healthcare systems.

First, they identified patients who underwent appendectomies and who were subsequently diagnosed with Parkinson’s disease six months after the surgery.

Among the 62,218,050 records from the database, the team identified 488,190 patients who had undergone appendectomies. There were 4,470 cases of Parkinson’s disease among those who had had appendectomies (.92%), and 177,230 cases among patients who had not (.29%).

Analysis of the prevalence of Parkinson’s disease in these populations showed that people who underwent an appendectomy had 3.19 times the risk of developing Parkinson’s disease compared to those who had not had the surgical procedure.

Researchers also found that the risk of developing Parkinson’s disease was similar across all age groups, regardless of gender or ethnicity.

“This research shows a clear relationship between the appendix, or appendix removal, and Parkinson’s disease, but it is only an association,” Sheriff said. “Additional research is needed to confirm this connection and to better understand the mechanisms involved.”

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Milk Linked to Greater Risk of Parkinson’s, Swedish Study Shows

milk risk factor

Consumption of more than 40 milliliters (1.3 ounces) of milk per day is associated with an increased risk of developing Parkinson’s disease. Still, dietary intake of yogurts or soured milk does not pose a risk, results from a large-scale Swedish study show.

The study “Milk, Yogurt, and Soured Milk Consumption and Risk of Parkinson’s Disease,” will be presented Erik Olsson, PhD, an associate professor at Uppsala University, during the 14th International Conference on Alzheimer’s and Parkinson’s Diseases and related neurological disorders, March 26-31, in Lisbon, Portugal.

Dairy products are widely consumed worldwide and could be important contributors for the development of human disease.

Previous studies have suggested consuming dairy products could be linked to an increased risk of Parkinson’s disease, particularly among men.

More recently, a study has shown that total dairy intake was not associated with a significant risk of Parkinson’s. However, daily consumption of low-fat or skim milk instead of full-fat milk was linked to a 39% higher chance of Parkinson’s disease.

To further explore this issue, Swedish researchers reviewed the incidence of Parkinson’s disease in 81,889 adults during a mean follow-up period of 13.9 years. None of the participants had Parkinson’s when the study started in 1997, and they all answered a questionnaire about dietary regimens and food intake frequency.

A total of 1,251 cases of Parkinson’s disease were reported among this population, according to information from the Swedish National Patient and Cause of Death Registers.

Analysis of the dietary patterns of this population revealed that people who consumed 40 milliliters (ml) or more of milk per day had increased risk of having Parkinson’s disease.

In particular, individuals who drank 40 to 159 ml per day of milk had a 30% higher risk of developing Parkinson’s, compared to people who had low daily milk intake (less than 40 ml per day). The risk increased similarly for people who consumed even higher amounts of milk, with 25%, 33%, and 33% higher risk for 160-200 ml, 201-400 ml, or more than 400 ml per day of milk.

In contrast, researchers did not find any significant association between intake of yogurt or soured milk and long-term risk of developing Parkinson’s disease.

These risk estimates did not change when the team analyzed the data according to participants’ gender, with no differences found between men and women.

“Findings from this cohort study indicate that consumption of milk, but not soured milk and yogurt, is associated with an increased risk of Parkinson’s disease,” researchers concluded.

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Study Examines Risk Factors for Impulse Control Disorders in Parkinson’s Patients

impulse control disorders

Use of dopamine agonists, earlier disease onset, being male, and having personality traits such as impulsiveness and high novelty-seeking are among the risk factors for developing impulse control disorders (ICDs) in people with Parkinson’s, according to a review study.

The research, “Impulse control disorders in Parkinson’s disease: A systematic review on risk factors and pathophysiology,” was published in the Journal of the Neurological Sciences.

ICDs are characterized by failure to resist an impulse, drive, or temptation to perform a risky behavior, a growing sense of tension before performing the behavior, and a sense of pleasure while doing it.

In people with Parkinson’s, ICDs may result from treatments intending to increase the levels of dopamine in the brain. Despite their impact on patients’ quality of life, studies about ICDs in this patient population are scarce.

Aiming to address this gap, a research team from IRCCS Centro Neurolesi “Bonino Pulejo”, in Italy, conducted a systematic review of the potential risk factors for the development of ICDs in people with Parkinson’s, including the effects of dopaminergic treatment. Three online databases were used covering studies published from January 2000 to July 2018.

According to research published in 2003 and 2008, the prevalence of gambling, compulsive sexual behavior, and compulsive shopping is 1.7-7.0%, 2.0–4.0%, and 0.4-3.0%, respectively. The 2003 study found one or more ICDs in 13.6% of patients, which included binge eating and hypersexuality. Recent epidemiological studies have indicated that the prevalence of ICDs is 7.2% in patients with Parkinson’s, but only 1% in controls (participants who did not have Parkinson’s.

Specifically, for example, although binge eating typically leads to weight gain, people with Parkinson’s commonly lose weight, which is attributed to swallowing difficulties (dysphagia) and dyskinesia (involuntary, jerky movements).

Slot machine gambling has been identified as the most common form of pathological gambling among these patients. Major depression in middle-aged men has been reported as a comorbidity of pathological gambling, with common genetic factors.

Patients also have an increased risk of developing dopamine dysregulation syndrome, which results from unregulated self-administration and dependence on dopaminergic treatment. “Patients increase drugs doses spontaneously and progressively and this is often associated to behavioral and mood disorders, such as hallucinations, manic states, aggression, psychomotor agitation and delusions,” researchers explained.

Developing addiction-like behavior has been associated with the type, dose and duration of dopaminergic treatment, in particular dopamine agonists.

A 2006 study showed a correlation between earlier onset of Parkinson’s and earlier appearance of motor fluctuations, dyskinesia and psychiatric symptoms. Also, a study with 3,090 patients indicated that greater impulsive choice, faster reaction time and impulsive decisions are among the potential factors for the development of ICDs, although Parkinson’s patients are thought to have increased caution and be risk-averse prior to diagnosis.

Comparing to women, men not only have higher frequency of ICDs, but also show six-times greater difficulty managing them, as shown in a 2012 study. Other factors shown to associate with ICDs in Parkinson’s include sleep impairment, substance abuse, high novelty-seeking, impulsiveness, aggressiveness, cigarette smoking, having more formal education, and being unmarried.

As for brain pathways underlying the development of ICDs, dysregulation of the mesolimbic circuit (responsible for reward learning and the mesocortical pathway (responsible for executive decision-making) leads to impulsive and compulsive behaviors.

Upon exposure to a reward, a brain area called the ventral striatum is activated, prompting a strong emotional response and dopamine release. This behavior ultimately may become compulsive, being reinforced by the dorsal striatum.

Two types of dopamine receptors — D1 and D2 — are involved in the connections between the striatum and the globus pallidus (a part of the brain’s basal ganglia) and subsequently the substantia nigra, a major brain region involved in Parkinson’s disease.

These receptors, and their pathways, have opposing roles in reward-based decision making, either stimulation (D1) or suppression (D2).

The researchers noted that standardized tests to evaluate the type and severity of ICDs are still lacking. Also, consistent use of international criteria for Parkinson’s diagnosis and prospective studies with larger samples are still needed to more accurately determine risk factors for ICDs among these patients.

“A better assessment of the behavioral disorders of [Parkinson’s] may be useful in the rehabilitative intervention for increasing the quality of life,” researchers concluded.

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Cancer Patients Have Lower Risk of Developing Parkinson’s Disease, Study Suggests

cancer, Parkinson's risk

Cancer patients appear to have a lower risk of developing Parkinson’s disease, even when taking into account important risk factors and overall survival, a study has found.

The study, “Cancers Preceding Parkinson’s Disease after Adjustment for Bias in a Danish Population-Based Case-Control Study,” was published in Neuroepidimiology.

Previous studies have shown that cancer patients are less likely to develop Parkinson’s during their lifetime than the general population. However, it is unclear whether this could be caused by the negative association between Parkinson’s disease and smoking, when, for many cancers, smoking is a known risk factor, or simply by the fact that most cancer patients do not survive long enough to reach a stage in which they are more likely to develop Parkinson’s.

Researchers at the University of California Los Angeles carried out a large population-based case-control study in Denmark (PASIDA) to investigate if cancer correlated with a lower risk of Parkinson’s disease, even after normalizing important risk factors, such as smoking, physical activity, and survival bias.

The study involved a total of 1,813 patients with Parkinson’s disease and 1,887 age- and sex-matched individuals without Parkinson’s used as controls.

Demographic analysis showed the percentage of non-smokers was higher in the group of Parkinson’s patients (49.6%) than in controls (35.3%). Conversely, the incidence of cancer was lower among Parkinson’s patients (3.8%) than in controls (4.2%), a difference that was even more pronounced when comparing the incidence of smoking-related cancers (1.7% versus 2.2%).

Apart from skin and breast cancer, further analysis showed a negative correlation between Parkinson’s disease and all types of cancers, including those related and not related to smoking. Even after normalization for risk factors and cancer patients’ survival bias, the negative association between Parkinson’s disease and cancer remained the same.

“Since PD [Parkinson’s disease] cases stop smoking many years prior to PD diagnosis, one might say that ‘PD prevents smoking’ and thus reduces the risk of smoking-related cancers and mortality. [However,] in PASIDA adjustment for pack-years of smoking did not change the observed associations between cancer and PD, which suggested that smoking is unlikely to be a strong confounder between cancer and PD,” the researchers wrote.

“In conclusion, our study suggested a lower frequency of most cancers preceding PD diagnosis after adjustment for major lifestyle factors. Our bias analysis indicated that survival bias minimally impacts the observed associations,” they added.

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Gout May Increase Parkinson’s Risk in Older People, Study of US Medicare Data Suggests

gout, Parkinson's risk

Gout appears to be associated with a higher risk of incident Parkinson’s disease in older adults, according to a study that looked at Medicare data in the U.S.

The study, “Gout and the risk of Parkinson’s disease in older adults: a study of U.S. Medicare data” was published in BMC Neurology.

Parkinson’s disease is a progressive neurological disorder that mainly affects motor function due to the loss of nerve cells in the brain that produce dopamine. When dopamine-producing neurons die, it causes symptoms such as tremors, stiffness, and balance problems.

About 1 percent of the population older than 60 are diagnosed with Parkinson’s. Due to this low incidence, risk factors for the disease have not been fully explored. It is known, however, that herbicide or pesticide exposure, along with hypertension, are potential risk factors for developing Parkinson’s. Inversely, use of statins (lipid-lowering medicines) and smoking are thought to lower the risk of developing the disease.

Previous studies have attempted to associate the levels of urate — a salt derived from uric acid — in the blood with the risk of developing Parkinson’s. Urate has an antioxidant effect that researchers think may help prevent the disease. As a result, lower levels of serum urate could lead to a higher Parkinson’s prevalence. However, so far, studies have not been able to confirm this association.

Gout is an inflammatory arthritis disease caused by increased oxidative stress and chronic inflammation, factors that can potentially increase the risk for Parkinson’s disease. Oxidative stress is an imbalance between the production of free radicals and the ability of cells to detoxify them. These free radicals or reactive oxygen species are harmful to cells and are associated with a number of diseases.

However, in a patient who has gout, serum urate levels are actually increased. “Acute and chronic inflammatory state in gout might potentially negate the anti-oxidant effects of urate, if one exists physiologically,” the researchers wrote.

Whether there is an association between urate and Parkinson’s risk in gout patients is still a matter of controversy.

In this study, researchers at the University of Alabama at Birmingham aimed to clarify the existence of a possible association between gout and Parkinson’s, taking into account other known risks for the disease such as age, sex, hypertension, hyperlipidemia (high levels of fat, also called lipids, in the blood), statin use, and demographic variables.

Using a random sample encompassing 5% of Medicare claims data, acquired from 2006 to 2012, a total of 1.72 million people — 1.63 million without gout and 94,133 with gout — were analyzed. Their mean age was 75.3 years, 58% were female, 36% were white, and they had a mean Charlson-Romano comorbidity index score — which predicts 10-year mortality — of 1.6.

The analysis was adjusted for statin use and cardiovascular disease, two potential confounding variables of Parkinson’s risk, as well as for the use of urate-lowering therapy.

A total of 22,636 people developed incident Parkinson’s disease — 21,507 without gout and 1,129 with gout. Older age, male gender, white race, and higher Charlson-Romano comorbidity index score were associated with a higher risk of Parkinson’s.

The analysis revealed that gout was independently linked to a 1.14 times higher risk of Parkinson’s. The risk differed significantly by age, with patients between the ages of 65 and 75 having the highest risk (1.27 times higher) and those older than 85 having a smaller risk (0.97). There was no risk association with gender or race/ethnicity for gout patients with incident Parkinson’s.

“Gout is associated with a modest increase in the risk of Prkinson’s for adults 65 years or older as a group, independent of other factors,” the researchers wrote, concluding that the “mechanisms of this increased risk of Parkinson’s in patients with gout needs to be investigated further.”

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Older IBD Patients Show Increased Risk for Parkinson’s Disease, Study Suggests

IBD risk factor

Older patients with inflammatory bowel disease (IBD) are more likely to develop Parkinson’s disease than those without the condition, a meta-analysis suggests.

Whether the same association exists for younger patients — ages 59 or younger — remains to be determined, according to the researchers.

The study, “Older patients with IBD might have higher risk of Parkinson’s disease,” was published in the journal Gut.

The chronic activation of pro-inflammatory mechanisms, which occurs in autoimmune conditions, has been increasingly recognized as a critical contributor of neurodegenerative disorders.

Studies suggest that this may happen due to the “gut-brain axis” — the two-way communication between the nervous system and the intestine that monitors gut function and links certain regions of the brain to intestinal functions, such as immune activation or intestinal permeability.

In line with the findings, some studies have already reported that patients with IBD — an autoimmune condition characterized by chronic inflammation of the gut — are 22-41% more likely to develop Parkinson’s than those without IBD.

However, a case-control study that examined Medicare data from 89,790 Parkinson’s cases and 118,095 population-based controls suggested that IBD actually reduced the risk for Parkinson’s by 15%.

To clarify this association, a team at Sichuan University in China reviewed all studies investigating the link between IBD and risk of Parkinson’s. Five studies met the inclusion criteria defined by the team, including a total of 9,174,766 participants.

Overall, IBD patients did not have a significantly higher risk of Parkinson’s than reference individuals, nor did patients with ulcerative colitis or Crohn’s disease — the two main forms of IBD — when examined individually.

However, patients 60 years or older were found to have a 32% higher risk of developing Parkinson’s. Patients 50 years or younger did not show this association, the researchers said.

“Our meta-analysis showed that patients with IBD did not have an increased risk of PD; however, subgroup analysis with cohort studies showed that they might be associated with increased risk of PD,” the researchers wrote.

“Age has been regarded as an important risk factor for Parkinson’s disease,” they added, but the findings suggest that “age at IBD diagnosis might be a risk factor of Parkinson’s disease.”

Interestingly, the team found that some studies reported medication-related side effects in the IBD population that resembled parkinsonism in the older population.

“It is necessary to take it into consideration whether older people will take more medications, and whether these medications lead to a higher risk of Parkinson’s also needs further studies to verify in the future,” they said.

Additional well-designed observational studies are still warranted to further explore the risk of Parkinson’s disease within the younger IBD population, the team noted.

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Taste, Smell Impairments May Help Identify People at Risk for Parkinson’s, Study Suggests

taste and smell impairment

Impaired sense of smell or taste can raise a person’s risk of developing Parkinson’s disease 2.5 times, a study suggests.

The study, “Incidence of Parkinson’s disease in a large patient cohort with idiopathic smell and taste loss,” was published in the Journal of Neurology.

Currently, Parkinson’s disease is diagnosed mainly on the assessment of patients’ motor symptoms and their severity. However, evaluation scales can be subjective and might fail to detect small changes.

Non-motor symptoms have gained increased attention because of their potential to anticipate Parkinson’s-related motor manifestations. Approximately 90% of Parkinson’s patients have altered smell sensitivity during the disease’s initial and moderate stages, thought to be partly because of brain connectivity changes.

To explore the incidence and diagnostic potential of smell and taste disorders in Parkinson’s disease, researchers reviewed the clinical records of 474 people who had been diagnosed with smell and taste loss of unknown cause.

Patients diagnosed and followed over a period of 15 years at the Smell and Taste Clinic in Dresden, Germany, were interviewed by phone using a standardized questionnaire to record their condition and clinical history.

At the time of the first assessment at the clinic, patients had already experienced reduced or lost  odor and taste sensitivity for a mean period of 4.6 years. Onset of olfactory (smell) disturbances was in general noticed at a mean age of 57.9 years; gustatory (taste) disorders, 59.3 years.

Of the 474 participants, 14.3% had a normal sense of smell, 40.5% had reduced, and 45.1% had complete loss of smell. Regarding taste, 90.1% of the participants had normal sensation, 9.5% had reduced, and 0.4% had complete loss of taste.

Collectively, 242 people were diagnosed with a qualitative olfactory or gustatory disorder, of whom 21.1% had parosmia (distortions of the sense of smell), 32.9% had phantosmia (olfactory hallucinations), and 7.6% had parageusia (distortions of the sense of taste).

Participants’ clinical reports revealed that 45 (9.5%) had developed Parkinson’s disease after the initial idiopathic smell and/or taste loss diagnosis.

Six of the Parkinson’s patients had combined olfactory and gustatory disorders at the time of diagnosis, whereas 38 had pure olfactory disorders and one patient had a pure gustatory disorder.

The frequency of taste disorders was similar between those with and without Parkinson’s. In contrast, Parkinson’s patients had a higher prevalence of initial complete loss of smell compared to those without the disease.

The team did not find a significant association between taste or smell loss and the development of the disease. Still, patients who developed Parkinson’s reported a decrease in olfactory and gustatory function more frequently than non-Parkinson’s patients.

Researchers found that “patients with a decrease in olfactory or gustatory function developed Parkinson’s with a significantly higher rate compared to patients with a stable smell or taste function.” Overall, impaired smell or taste sense increased the risk of developing Parkinson’s disease 2.47 times.

“Risk stratification might be considerably improved by correct diagnostic allocation of smell and taste loss, the use of both olfactory and gustatory testing, and subsequent long-term monitoring of these functions,” researchers said.

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Study Outlines Risk Factors for Levodopa-induced Dyskinesia in Newly Diagnosed PD Patients

Parkinson's levodopa-induced dyskinesia

Severe motor, functional, and gait impairment; cumulative levodopa exposure; anxiety, and sex are among the risk factors for developing levodopa-induced dyskinesia (LID) in people newly diagnosed  with Parkinson’s disease, according to results from the Parkinson’s Progression Markers Initiative (PPMI).

The research, “Risk factors of levodopa-induced dyskinesia in Parkinson’s disease: results from the PPMI cohort,” was published in the journal npj Parkinson’s Disease.

Long-term dopamine repletion therapy in Parkinson’s patients can lead to motor fluctuations, including dyskinesia — involuntary, jerky movements. According to observational studies, over 50% of Parkinson’s patients on levodopa — the gold-standard treatment for Parkinson’s — for more than five years develop LID.

Proposed risk factors for LID include levodopa dosage — associated with the loss of dopamine-producing neurons in the brain — treatment duration, low body weight, and being a woman. However, available studies have employed different methodological approaches and follow-up duration.

The PPMI is an ongoing, large-scale, collaborative study initiated in 2010 to identify markers of disease progression in de novo patients — newly diagnosed and still untreated. Patients’ clinical, neuroimaging and cerebrospinal fluid (the liquid surrounding the brain and the spinal cord)/blood biomarkers are collected yearly in this international study.

Analyzed biomarkers include the total amount of the tau protein as well as its altered (phosphorylated) version — which forms tangles inside neurons in Parkinson’s patients — total alpha-synuclein (the main component of Lewy bodies), and amyloid-beta (1-42), a protein that is also relevant in Alzheimer’s disease.

Researchers from Ospedale S. Maria della Misericordia, in Perugia, Italy, wanted to define factors predictive of LID development in de novo Parkinson’s patients.

Data from 423 patients were analyzed. Median follow-up duration was 4.6 years and average time to start dopaminergic therapy was one year.

A combination of factors, such as disease duration, anxiety — assessed with the State-Trait Anxiety Inventory (STAI) — and higher (worse) score on the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale (MDS-UPDRS) part III, which assesses motor function, predicted the initiation of dopaminergic therapy.

Overall, 109 of 390 patients analyzed experienced LID (27.9%), 33 of whom lacked data regarding levodopa treatment and/or LID onset. The median time to LID was 3.6 years (range 0.8-7.1 years), with a mean onset time of 5.81 years from Parkinson’s diagnosis, and an incidence rate of 64 per 1,000 person-years. This measure comprises actual follow-up duration in each patient and is higher with the length of the study.

Individual risk factors for LID development included being a woman, not being completely functional independent as measured by the modified Schwab & England Activities of Daily Living scale, higher MDS-UPDRS part III score, postural instability-gait disturbance (PIGD) or intermediate phenotype, higher DaTscan caudate asymmetry index — which reflects the difference in the levels of dopamine transport between two areas of the brain involved in motor control — higher genetic risk score, and anxiety.

Of note, no cerebral spinal fluid biomarker predicted LID development.

Researchers also found that the onset of dyskinesia was associated with depression and anxiety.

Combining all factors with an additional variable of 1,000 mg/day of levodopa equivalent daily dose — the amount of levodopa with a similar effect as the medication taken — was also found to be fairly accurate to predict dyskinesia onset.

“In summary, our findings indicate that data deriving from a large cohort of de novo PD patients monitored longitudinally are useful in understanding the composite aspects involved in the progression of disease,” researchers stated.

The team also said the findings may help “future design of both biomarker studies and randomized clinical trials.”

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