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Is the risk of motor neuron disease increased or decreased after cancer? An Australian case-control study.

ABSTRACT: Cancer appears to be inversely associated with both Alzheimer's and Parkinson's disease. The relationship between cancer and sporadic motor neuron disease (SMND), however, remains uncertain. Most previous cancer-SMND studies have been undertaken in northern hemisphere populations. We therefore undertook a case-control study to see if a link between cancer and SMND exists in an Australian population. A questionnaire was used to compare past cancer diagnoses in 739 SMND patients and 622 controls, recruited across Australia. Odds ratios with 95% confidence intervals were calculated to look for associations between cancer and SMND. A history of cancer was not associated either positively or negatively with a risk of subsequent SMND. This result remained when age, gender, smoking status, and the four SMND diagnostic subgroups were taken into account. No association was observed between SMND and specific tumours, including melanoma, a common malignancy in Australia. In conclusion, this Australian case-control study does not support an association between a past history of cancer and the development of SMND. This suggests that some pathogenetic mechanisms, such as apoptosis, are less relevant in SMND than in other neurodegenerative diseases where negative associations with cancer have been found.

SUBMITTER: Stoyanov A

PROVIDER: S-EPMC4110050 | biostudies-other | 2014

REPOSITORIES: biostudies-other

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Increased risk of sudden cardiac arrest in obstructive pulmonary disease: a case-control study.

Project description:BackgroundWe aimed to determine whether (1) patients with obstructive pulmonary disease (OPD) have an increased risk of sudden cardiac arrest (SCA) due to ventricular tachycardia or fibrillation (VT/VF), and (2) the SCA risk is mediated by cardiovascular risk-profile and/or respiratory drug use.MethodsA community-based case-control study was performed, with 1310 cases of SCA of the ARREST study and 5793 age, sex and SCA-date matched non-SCA controls from the PHARMO database. Only incident SCA cases, age older than 40 years, that resulted from unequivocal cardiac causes with electrocardiographic documentation of VT/VF were included. Conditional logistic regression analysis was used to assess the association between SCA and OPD. Pre-specified subgroup analyses were performed regarding age, sex, cardiovascular risk-profile, disease severity, and current use of respiratory drugs.ResultsA higher risk of SCA was observed in patients with OPD (n?=?190 cases [15%], 622 controls [11%]) than in those without OPD (OR adjusted for cardiovascular risk-profile 1.4 [1.2-1.6]). In OPD patients with a high cardiovascular risk-profile (OR 3.5 [2.7-4.4]) a higher risk of SCA was observed than in those with a low cardiovascular risk-profile (OR 1.3 [0.9-1.9]) The observed SCA risk was highest among OPD patients who received short-acting ?2-adrenoreceptor agonists (SABA) or anticholinergics (AC) at the time of SCA (SABA OR: 3.9 [1.7-8.8], AC OR: 2.7 [1.5-4.8] compared to those without OPD).ConclusionsOPD is associated with an increased observed risk of SCA. The most increased risk was observed in patients with a high cardiovascular risk-profile, and in those who received SABA and, possibly, those who received AC at the time of SCA.

| S-EPMC3675036 | biostudies-literature

Increased motor cortical facilitation and decreased inhibition in Parkinson disease.

Project description:ObjectiveTo identify the changes in motor cortical facilitatory and inhibitory circuits in Parkinson disease (PD) by detailed studies of their time courses and interactions.MethodsShort-interval intracortical facilitation (SICF) and short-interval intracortical inhibition (SICI) were measured with a paired-pulse paradigm using transcranial magnetic stimulation. Twelve patients with PD in both ON and OFF medication states and 12 age-matched healthy controls were tested. The first experiment tested the time course of SICF in PD and controls. The second experiment tested SICI at different times corresponding to SICF peaks and troughs to investigate whether SICI was affected by SICF.ResultsSICF was increased in PD OFF state and was reduced by dopaminergic medications. The reduction in SICF from the OFF to ON state correlated with the improvement in PD motor signs. SICI was reduced in PD OFF state and was only partially normalized by dopaminergic medications. At SICF peaks, improvement in SICI with medication correlated with improvement in PD motor sign. Principal component analysis showed that variations of SICF and SICI were explained by the same principal component only in the PD OFF group, suggesting that decreased SICI in the OFF state is related to increased SICF.ConclusionsMotor cortical facilitation is increased and inhibition is decreased in PD. Increased cortical facilitation partly accounts for the decreased inhibition, but there is also impairment in synaptic inhibition in PD. Increased cortical facilitation may be a compensatory mechanism in PD.

| S-EPMC3719423 | biostudies-literature

Affymetrix 6.0 study of sporadic motor neuron disease patients and controls.

Project description:This data was divided into three experiment sets: 1. A somatic study of sporadic motor neuron disease (SMND) brain samples that were compared to the blood from the same individual, normal control brains and disease control brans (Parkinson Disease patients); 2. A twin study comparing blood and other tissue samples from twins that were discordant for MND, concordant for MND and control twins and 3. A trio study of blood samples MND patients compared to their unaffected parents. Study 1: 36 sporadic motor neuron disease brain (lateral frontal cortex, Brodmann area 46), 34 matched sporadic motor neuron disease blood, 26 control brain (lateral frontal cortex, Brodmann area 46), 9 Parkinson Disease brain (disease controls, lateral frontal cortex, Brodmann area 46). Study 2 and study 3: 52 twin or trio blood, 4 twin hair, 1 twin sperm. 2 replicate twin blood and 1 replicate trio blood repeated at a different time. External control blood from Coriell GM15510 and GM10851.

2010-07-31 | E-GEOD-15826 | biostudies-arrayexpress

Decreased Risk of Parkinson's Disease After Rheumatoid Arthritis Diagnosis: A Nested Case-Control Study with Matched Cases and Controls.

Project description:BackgroundRheumatoid arthritis (RA) and the genetic risk landscape of autoimmune disorders and Parkinson's disease (PD) overlap. Additionally, anti-inflammatory medications used to treat RA might influence PD risk.ObjectiveTo use a population-based approach to determine if there is an association between pre-occurring rheumatoid arthritis (RA) and later-life risk of PD.MethodsThe study population was 3.6 million residents of Sweden, who were alive during part or all of the follow-up period; 1997-2016. We obtained diagnoses from the national patient registry and identified 30,032 PD patients, 8,256 of whom each was matched to ten controls based on birth year, sex, birth location, and time of follow-up. We determined the risk reduction for PD in individuals previously diagnosed with RA. We also determined if the time (in relation to the index year) of the RA diagnosis influenced PD risk and repeated the analysis in a sex-stratified setting.ResultsIndividuals with a previous diagnosis of RA had a decreased risk of later developing PD by 30-50% compared to individuals without an RA diagnosis. This relationship was strongest in our conservative analysis, where the first PD diagnosis occurred close to the earliest PD symptoms (odds ratio 0.47 (CI 95% 0.28-0.75, p = 0.0006); with the greatest risk reduction in females (odds ratio 0.40 (CI 95% 0,19-0.76, p = 0.002).DiscussionOur findings provide evidence that individuals diagnosed with RA have a significantly lower risk of developing PD than the general population. Our data should be considered when developing or repurposing therapies aimed at modifying the course of PD.

| S-EPMC8150472 | biostudies-literature

Parkinsonian Syndromes in Motor Neuron Disease: A Clinical Study

Project description:Background Parkinsonian syndromes may rarely occur in motor neuron disease (MND). However, previous studies are heterogeneous and mostly case reports or small case series. Therefore, we aimed to identify and characterize patients with concurrent parkinsonian syndromes extracted from a cohort of 1,042 consecutive cases diagnosed with MND at a tertiary Italian Center. Methods Diagnosis of Parkinson's disease (PD), progressive supranuclear palsy (PSP) and corticobasal syndrome (CBS) was made according to current criteria. Clinical characterization included: upper and lower motor neuron disease features, typical and atypical parkinsonian features, oculomotor disorders, cognitive testing, MRI features, and, when available molecular neuroimaging. Genetic testing was carried out for major MND and PD-associated genes. Results Parkinsonian syndromes were diagnosed in 18/1042 (1.7%) of MND patients (7 PD, 6 PSP, 3 CBS, 2 other parkinsonisms). Based on phenotype, patients could be categorized into amyotrophic lateral sclerosis (ALS)-parkinsonism and primary lateral sclerosis (PLS)-parkinsonism clusters. Across the whole database, parkinsonism was significantly more common in PLS than in other MND phenotypes (12.1 vs. 1.1%, p = 5.0 × 10−10). MND patients with parkinsonian features had older age of onset, higher frequency of oculomotor disorders, cognitive impairment, and family history of parkinsonism or dementia. Two patients showed pathogenic mutations in TARDBP and C9orf72 genes. Conclusion Specific patterns in MND-parkinsonism were observed, with PLS patients often showing atypical parkinsonian syndromes and ALS patients more frequently showing typical PD. Systematic clinical, genetic, and neuropathologic characterization may provide a better understanding of these phenotypes.

| S-EPMC9271964 | biostudies-literature

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Project description:Spinal muscular atrophy (SMA) is caused by depletion of the ubiquitously expressed survival motor neuron (SMN) protein, with 1 in 40 Caucasians being heterozygous for a disease allele. SMN is critical for the assembly of numerous ribonucleoprotein complexes, yet it is still unclear how reduced SMN levels affect motor neuron function. Here, we examined the impact of SMN depletion in Caenorhabditis elegans and found that decreased function of the SMN ortholog SMN-1 perturbed endocytic pathways at motor neuron synapses and in other tissues. Diminished SMN-1 levels caused defects in C. elegans neuromuscular function, and smn-1 genetic interactions were consistent with an endocytic defect. Changes were observed in synaptic endocytic proteins when SMN-1 levels decreased. At the ultrastructural level, defects were observed in endosomal compartments, including significantly fewer docked synaptic vesicles. Finally, endocytosis-dependent infection by JC polyomavirus (JCPyV) was reduced in human cells with decreased SMN levels. Collectively, these results demonstrate for the first time, to our knowledge, that SMN depletion causes defects in endosomal trafficking that impair synaptic function, even in the absence of motor neuron cell death.

| S-EPMC4968725 | biostudies-literature

NINDS Inherited Forms of Motor Neuron Disease Study

Project description:NINDS Inherited Forms of Motor Neuron Disease Study

| PRJNA377929 | ENA

Affymetrix 6.0 study of sporadic motor neuron disease patients and controls.

2010-07-31 | GSE15826 | GEO

EAEC case-control study

Project description:Virulence factor characterization of EAEC strains

| PRJEB16673 | ENA

Prefrontal cortical thickness in motor neuron disease.

Project description:To examine whether the distribution of prefrontal cortical thickness in patients with motor neuron disease is normal or bimodal and how it compares to the normal population.158 patients with motor neuron disease (MND) and 86 healthy controls (HC) were enrolled in a prospective, two-center study with a common structural MRI protocol. Cortical thickness measures were extracted for the prefrontal cortex, premotor cortex, motor cortex, and occipital cortex using FreeSurfer, adjusted for age and sex, and tested for normality of distribution.Cortical thickness measures of the bilateral prefrontal, premotor, motor, and occipital cortex were normally distributed in patients and healthy controls. MND-related cortical thinning was observed in the right motor cortex (p?=?0.002), reflected in a significantly higher proportion of MND cases being worse than -1 standard deviation of the healthy control mean: 29.1% in the right motor cortex (p?=?0.002). Cortical thinning of the left motor cortex was a function of clinical phenotype and physical disability. Left prefrontal cortical thickness was reduced in patients with additional cognitive and/or behavioural deficits compared to MND patients without cognitive deficits. Prefrontal, premotor, motor, and occipital cortical thickness was related to patients' general cognitive abilities.The study shows that prefrontal cortical thickness in MND is normally distributed but shifted towards thinner cortex in MND patients with cognitive and/or behavioural impairment. The distribution of thickness values did not indicate the assumption of a bimodal distribution although patients with comorbid cognitive deficits are more likely to suffer from prefrontal cortical thinning.

| S-EPMC5987868 | biostudies-other

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