Bicycling for Rehabilitation of Persons With Parkinson Disease: A Scoping Review.

BACKGROUND AND PURPOSE: Exercise is beneficial for persons with Parkinson disease (PwPD). The overarching purpose of this scoping review was to provide guidance to clinicians and scientists regarding current evidence for bicycling exercise for PwPD. A scoping review was conducted to examine the heterogeneous literature on stationary bicycling for PwPD to reduce motor symptoms and body function structure impairments, improve activities and motor performance, and reduce disease severity. METHODS: The Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) guidelines were followed. PubMed, CINAHL, and PEDro were searched from inception to January 23, 2023. Articles reporting original data on relevant outcome measures were included. Search results were screened and articles were extracted. Data were analyzed quantitatively with percentages of significant and clinically meaningful findings and qualitatively to extract themes. RESULTS: Bicycling was categorized using bicycle types (assisted, nonassisted) and training modes (speed, aerobic, force). A high percentage of the 34 studies showed statistical significance for reducing motor symptoms (83%), body function structure impairments (78%), disease severity (82%), and improving activities (gait 72%, balance 60%). Clinically meaningful findings were achieved in 71% of the studies for reduction in disease severity and in 50% for improving gait. DISCUSSION AND CONCLUSIONS: The literature on bicycling for PwPD has evolved from speed to aerobic studies. The terminology describing types of bicycling was simplified. Of all the outcomes reported, reduction of disease severity achieved the highest frequency of clinical meaningful improvements. Bicycling was comparable with other forms of aerobic training for walking speed and endurance. Opportunities for translation to practice and research are presented.

Expanding student nurse placement activity in Welsh care homes: An evaluation study.

AIM: Expanding and sustaining student nurse placements outside of the acute sector is a universal challenge. This paper aims to evaluate the Care Home Education Facilitator Role introduced in one area of Wales, United Kingdom, and to report on the outcomes achieved from this novel role. METHODS: Semi-structured interviews were undertaken with key stakeholders including the Care Home Education Facilitator postholder leading the pilot, care home managers, higher education institutions' placement managers/coordinators, student nurses and national health service staff. RESULTS: Five key areas were identified, which included timing of introducing the post and establishing a clear rationale and understanding of the intention of the role. The benefits, challenges and suggested improvements to the Care Home Education Facilitator initiative are provided. CONCLUSION: Introducing the role of the Care Home Education Facilitator to work closely with key stakeholders resulted in increased placements for student nurses, but investing time in developing relationships with these stakeholders was critical to the success of the role.

Modification of Huntington's disease by short tandem repeats.

Expansions of glutamine-coding CAG trinucleotide repeats cause a number of neurodegenerative diseases, including Huntington's disease and several of spinocerebellar ataxias. In general, age-at-onset of the polyglutamine diseases is inversely correlated with the size of the respective inherited expanded CAG repeat. Expanded CAG repeats are also somatically unstable in certain tissues, and age-at-onset of Huntington's disease corrected for individual HTT CAG repeat length (i.e. residual age-at-onset), is modified by repeat instability-related DNA maintenance/repair genes as demonstrated by recent genome-wide association studies. Modification of one polyglutamine disease (e.g. Huntington's disease) by the repeat length of another (e.g. ATXN3, CAG expansions in which cause spinocerebellar ataxia 3) has also been hypothesized. Consequently, we determined whether age-at-onset in Huntington's disease is modified by the CAG repeats of other polyglutamine disease genes. We found that the CAG measured repeat sizes of other polyglutamine disease genes that were polymorphic in Huntington's disease participants but did not influence Huntington's disease age-at-onset. Additional analysis focusing specifically on ATXN3 in a larger sample set (n = 1388) confirmed the lack of association between Huntington's disease residual age-at-onset and ATXN3 CAG repeat length. Additionally, neither our Huntington's disease onset modifier genome-wide association studies single nucleotide polymorphism data nor imputed short tandem repeat data supported the involvement of other polyglutamine disease genes in modifying Huntington's disease. By contrast, our genome-wide association studies based on imputed short tandem repeats revealed significant modification signals for other genomic regions. Together, our short tandem repeat genome-wide association studies show that modification of Huntington's disease is associated with short tandem repeats that do not involve other polyglutamine disease-causing genes, refining the landscape of Huntington's disease modification and highlighting the importance of rigorous data analysis, especially in genetic studies testing candidate modifiers.

Genetic modifiers of somatic expansion and clinical phenotypes in Huntington's disease reveal shared and tissue-specific effects.

Huntington's disease (HD), due to expansion of a CAG repeat in HTT , is representative of a growing number of disorders involving somatically unstable short tandem repeats. We find that overlapping and distinct genetic modifiers of clinical landmarks and somatic expansion in blood DNA reveal an underlying complexity and cell-type specificity to the mismatch repair-related processes that influence disease timing. Differential capture of non-DNA-repair gene modifiers by multiple measures of cognitive and motor dysfunction argues additionally for cell-type specificity of pathogenic processes. Beyond trans modifiers, differential effects are also illustrated at HTT by a 5'-UTR variant that promotes somatic expansion in blood without influencing clinical HD, while, even after correcting for uninterrupted CAG length, a synonymous sequence change at the end of the CAG repeat dramatically hastens onset of motor signs without increasing somatic expansion. Our findings are directly relevant to therapeutic suppression of somatic expansion in HD and related disorders and provide a route to define the individual neuronal cell types that contribute to different HD clinical phenotypes.