New testing method developed for patients with Parkinson's disease

Nearly all diagnostic testing for Parkinson’s disease revolves around how a patient moves and requires the patient to walk for extensive distances and amounts of time, however, this can be an uncomfortable process. An international team of researchers based in Saudi Arabia and Sweden have proposed a new kind of computational analysis based on less physically demanding testing. They published their findings in the November 2019 issue of IEEE/CAA Journal of Automatica Sinica, a joint publication of the Institute of Electrical and Electronics Engineers (IEEE) and the Chinese Association of Automation (CAA). In this experiment, subjects press one or two buttons on a device such as an Iphone as fast as possible for a short period of time. The team took these data and analyzed them through fuzzy recurrence plots, which take multiple short-time series data points and translate them into a two-dimensional grey-scale images of texture. In the image, related points appear as a dense grey, with more disparate data points becoming fuzzier. The algorithm used for the fuzzy recurrence plots learns how the data points connect and can help provide differences and similarities in subject groups such as people with early Parkinson's disease and those without. The team plans to further study the use of fuzzy recurrence plots and improve the algorithm to better determine a subject's disease state. They also plan to extend the research to study gait dynamics of patients with Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis, also known as Lou Gehrig's disease.

Huntington’s organoids are abnormal early on

Investigators at the Agency for Science, Technology and Research (A*STAR) have reported that brain organoids developing from iPSCs with the CAG expansion that causes Huntington’s disease showed abnormalities very early in development. Huntington’s disease typically becomes clinically evident in late middle age, and the assumption has been that it is a neurodegenerative disorder, but it does not have a developmental component. Recent studies, however, have suggested a neurodevelopmental component as well. The authors tested this possibility in organoid models and found that cells with the CAG expansion had an imbalance between proliferation and differentiation early in development. They concluded that their results “further support the view that HD, at least in its early-onset forms, may not be a purely neurodegenerative disorder, and that abnormal neurodevelopment may be a component of HD pathophysiology.” The work was posted by its authors on the Biorxiv preprint server Nov. 26, 2019.

DNA circles drive neuroblastomas

Scientists at Memorial Sloan-Kettering Cancer Center and Humboldt University Berlin have shown that extrachromosomal circular DNAs were “an unanticipated major source of somatic rearrangements, contributing to oncogenic remodeling through chimeric circularization and reintegration of circular DNA into the linear genome” of neuroblastoma cells. The presence of circular DNA, and even the circularization of whole chromosomes, is a known phenomenon in tumor cells. For neuroblastoma it was first described more than 50 years ago. However, neither its extent nor its functional consequences have been analyzed in detail. The researchers used DNA and RNA sequencing to investigate its potential role as a cancer driver. They showed that cancer-causing rearrangements could result from DNA that first circularized, and then reintegrated into the linear genome. Such rearrangements correlated with poor clinical prognosis. “It is highly probable that circle-derived rearrangements represent an ongoing mutagenic process,” the authors wrote. Their work appeared in the Dec. 16, 2019, online issue of Nature Genetics.

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