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Immune cells in blood influence the brain during early development of Parkinson s disease

 E-Mail Parkinson s disease has always been considered a brain disorder. However, new research reveals a close link between the disease and certain immune cells in the blood. Researchers from Aarhus University have taken the first step on a path which can lead to new ways of understanding and, in the long term, possibly treating this widespread disease that affects not only motor functions but also cognition and emotions. We know that Parkinson s disease is characterized by an inflammation in the brain, and that this is crucial for the progression of the disease. But in the study, our interest has been focused on the immune cells found outside the brain, explains Marina Romero-Ramos, who is associate professor at the Department of Biomedicine at Aarhus University.

Antisense oligonucleotides as a feasible therapy to treat MECP2 duplication disorder

 E-Mail Many cognitive neurodevelopmental disorders are a result of too many or too few copies of certain genes or chromosomes. To date, no treatment options exist for this class of disorders. MECP2 duplication syndrome (MDS) is one such disorder that primarily affects boys and results from a duplication spanning the methyl-CpG binding protein 2 (MECP2) locus located on the X chromosome. A preclinical study published from the laboratory of Dr. Huda Zoghbi, professor at Baylor College of Medicine and director of the Jan and Dan Duncan Neurological Research Institute at Texas Children s Hospital, provides experimental evidence that supports the use of antisense oligonucleotides as a feasible strategy to treat MDS. The study also offers crucial insights into the pharmacodynamics of this approach, which will serve as an important guide for the design and implementation of future clinical trials for this disorder. The study appears in the journal

Cancer guardian breaks bad with one switch

 E-Mail IMAGE: A model produced by scientists at Rice University shows the conformational changes caused by a mutation in the cancer-fighting p53 protein. At top left, the red box highlights the aggregation-prone. view more  Credit: Kolomeisky Research Group/Rice University HOUSTON - (March 4, 2021) - A mutation that replaces a single amino acid in a potent tumor-suppressing protein turns it from saint to sinister. A new study by a coalition of Texas institutions shows why that is more damaging than previously known. The ubiquitous p53 protein in its natural state, sometimes called the guardian of the genome, is a front-line protector against cancer. But the mutant form appears in 50% or more of human cancers and actively blocks cancer suppressors.

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