Tuesday, 27 December 2011

Olfaction in Parkinson's disease and related disorders

Neurobiol Dis. 2011 Dec 20. [Epub ahead of print]
Doty RL.
Olfactory dysfunction is an early 'pre-clinical' sign of Parkinson's disease (PD). The present review is a comprehensive and up-to-date assessment of such dysfunction in PD and related disorders. The olfactory bulb is implicated in the dysfunction, since only those syndromes with olfactory bulb pathology exhibit significant smell loss. The role of dopamine in the production of olfactory system pathology is enigmatic, as overexpression of dopaminergic cells within the bulb's glomerular layer is a common feature of PD and most animal models of PD. Damage to cholinergic, serotonergic, and noradrenergic systems is likely involved, since such damage is most marked in those diseases with the most smell loss. When compromised, these systems, which regulate microglial activity, can influence the induction of localized brain inflammation, oxidative damage, and cytosolic disruption of cellular processes. In monogenetic forms of PD, olfactory dysfunction is rarely observed in asymptomatic gene carriers, but is present in many of those that exhibit the motor phenotype. This suggests that such gene-related influences on olfaction, when present, take time to develop and depend upon additional factors, such as those from aging, other genes, formation of α-synuclean- and tau-related pathology, or lowered thresholds to oxidative stress from toxic insults. The limited data available suggest that the physiological determinants of the early changes in PD-related olfactory function are likely multifactorial and may include the same determinants as those responsible for a number of other non-motor symptoms of PD, such as dysautonomia and sleep disturbances.

Incidence and mortality of Parkinson's disease in older Canadians

Parkinsonism Relat Disord. 2011 Dec 23. [Epub ahead of print]

Allyson Jones C, Wayne Martin WR, Wieler M, King-Jesso P, Voaklander DC.


School of Public Health, University of Alberta, Canada.


To estimate the age-specific incidence of Parkinson's disease (PD) in elderly persons in the Canadian province of British Columbia (BC). All-cause and injury mortalities and relative risk of death for those persons with PD were also examined.


A historical cohort study was conducted using 5 provincial administrative databases from 1991/92 to 2000/2001. A series of algorithms based on the databases were created for case ascertainment of PD for persons 65 years or older. Crude and age-specific incidence and mortality rates were calculated using person-years of follow-up as the denominator. The impact of PD on all-cause and injury mortalities was examined using multivariate Cox regression models to provide adjusted hazard ratios.


10,910 incidence cases over 6,051,682 person-years of follow-up were identified. The crude annual incidence rate was 252 per 100,000 person-years. Over the nine year period, age standardized incidence for males ranged from 207 to 396 per 100,000 person-years and 127 to 259 per 100,000 person-years for females. Persons with PD were at a 43% greater risk of all-cause mortality and specifically, 51% greater risk of injury mortality.


Incidence of PD is substantially higher in advanced age with age adjusted increases for both all-cause and injury mortalities. These findings also highlight falls as a primary factor for injury mortality in PD.

Sunday, 18 December 2011

Small study of caffeine in PD


"This is a small study of treatment with caffeine in Parkinson's. Previous studies suggest that people who drink coffee are less likely to be diagnosed with Parkinson's. Reasons for this observation include: 1) caffeine protects you against Parkinson's, 2) coffee delays the onset of Parkinson's or 3) people with early undiagnosed Parkinson's do not get the normal positive effect from coffee and therefore don't use it. Whatever the reason, caffeine remains a good candidate drug for treating Parkinson's. This small study shows some benefit from treatment with caffeine in certain aspects of the disease and not in others. It also suggests a dose that can be tolerated. Clearly larger studies are warranted."

Saturday, 17 December 2011


"I've been going through the participant feedback from the PREDICT PD study now that we have most of the results in. I will be posting selected feedback on this blog to try and answer outstanding questions from participants".

Tuesday, 6 December 2011

Dietary patterns and risk of Parkinson's disease: a case-control study in Japan

Background:  Nearly all epidemiologic studies examining the association between the risk of Parkinson's disease (PD) and diet have focused on single foods and specific nutrients. However, epidemiologic evidence for the association of dietary pattern with PD, namely the measurement of overall diet by considering the cumulative effects of nutrients is extremely limited. We conducted a hospital-based case-control study in Japan to examine the relationship between dietary patterns and the risk of PD. Methods:  Patients with PD diagnosed using the UK PD Society Brain Bank criteria (n = 249) and controls without neurodegenerative diseases (n = 368) were recruited. At the time of recruitment, dietary intake during the preceding 1 month was assessed using a validated, self-administered diet history questionnaire. Dietary patterns from 33 predefined food groups (energy-adjusted food g/day) were extracted by factor analysis. Results:  Three dietary patterns were identified: 'Healthy', 'Western' and 'Light meal' patterns. After adjustment for potential non-dietary confounding factors, the Healthy pattern, characterized by a high intake of vegetables, seaweed, pulses, mushrooms, fruits and fish, was inversely associated with the risk of PD with a border-line significance (P for trend = 0.06). Multivariate Odds ratio (95% confidence intervals) for PD in the highest quartile of the Healthy pattern was 0.54 (0.32-0.92) compared with the lowest quartile. No associations with PD were detected for the other two dietary patterns. Conclusion:  In this case-control study in Japan, a dietary pattern consisting of high intakes of vegetables, fruits and fish may be associated with a decreased risk of PD.

Sunday, 4 December 2011

Monoamine oxidase B inhibitors for the treatment of Parkinson's disease: a review of symptomatic and potential disease-modifying effects.


A. Schapira
CNS Drugs. 2011 Dec 1;25(12):1061-71.

Parkinson's disease is a disorder characterized pathologically by progressive neurodegeneration of the dopaminergic cells of the nigrostriatal pathway. Although the resulting dopamine deficiency is the cause of the typical motor features of Parkinson's disease (bradykinesia, rigidity, tremor), additional non-motor symptoms appear at various timepoints and are the result of non-dopamine nerve degeneration. Monoamine oxidase B (MAO-B) inhibitors are used in the symptomatic treatment of Parkinson's disease as they increase synaptic dopamine by blocking its degradation. Two MAO-B inhibitors, selegiline and rasagiline, are currently licensed in Europe and North America for the symptomatic improvement of early Parkinson's disease and to reduce off-time in patients with more advanced Parkinson's disease and motor fluctuations related to levodopa. A third MAO-B inhibitor (safinamide), which also combines additional non-dopaminergic properties of potential benefit to Parkinson's disease, is currently under development in phase III clinical trials as adjuvant therapy to either a dopamine agonist or levodopa. MAO-B inhibitors have also been studied extensively for possible neuroprotective or disease-modifying actions. There is considerable laboratory evidence that MAO-B inhibitors do exert some neuroprotective properties, at least in the Parkinson's disease models currently available. However, these models have significant limitations and caution is required in assuming that such results may easily be extrapolated to clinical trials. Rasagiline 1 mg/day has been shown to provide improved motor control in terms of Unified Parkinson's Disease Rating Scale (UPDRS) score at 18 months in those patients with early disease who began the drug 9 months before a second group. There are a number of possible explanations for this effect that may include a disease-modifying action; however, the US FDA recently declined an application for the licence of rasagiline to be extended to cover disease modification.

Thursday, 1 December 2011

NSAID use and the risk of Parkinson's

  1. C. Becker, 
  2. S. S. Jick, 
  3. C. R. Meier
  1. European Journal of Neurology, Nov. 2011

Background:  Previous epidemiologic studies have produced inconsistent findings regarding the association between the use of non-steroidal anti-inflammatory drugs (NSAIDs) and the risk of Parkinson disease (PD).
Methods:  We conducted a case–control analysis using the General Practice Research Database. Cases (≥40 years) had a new diagnosis of PD between 1994 and 2009. We matched four controls to each PD case on age, sex, general practice, and index date. Use of NSAIDs, aspirin, and acetaminophen was stratified by exposure timing and duration for both cases and controls. We calculated odds ratios (OR) using conditional logistic regression. For additional analyses, the index date was brought backward 1, 2, and 3 years, respectively.
Results:  We identified 4026 cases with an incident idiopathic PD diagnosis and 15 969 matched controls. Compared with patients without any previous prescription for NSAIDs, those with prior use had no increased risk of a PD diagnosis (OR 1.07, 95% CI 0.99–1.16). Long-term use (≥15 prescriptions) was associated with a slightly lower PD risk (adjusted OR 0.94, 95% CI 0.83–1.07). The relative PD risks of the use of aspirin or acetaminophen were not materially higher (PD risk of long-term use: adjusted ORs 1.16, 95% CI 1.03–1.30 and 1.15, 95% CI 1.02–1.30, respectively) compared with those for non-users. The risk estimate diminished toward the null in subsequent analyses with shifted index dates.
Conclusion:  In this large observational study with data from the UK primary care, the long-term use of NSAIDs, aspirin, or acetaminophen was not associated with a substantially altered risk of developing PD.

Peripheral Neuropathy and Parkinson's

Full Free Article

"This is a free article in this week's Neurology Journal. It is a study which looked at the relationship between Parkinson's and peripheral neuropathy. It was been written to explain to the public how this particular research study was performed."