Engineering 2D spin networks by on-surface encapsulation of azafullerene radicals in nanotemplates.

We present an efficient strategy for on-surface engineering of organic metal-free supramolecular complexes with long-term spin protection. By vacuum deposition of azafullerene (CN) monomers on a pre-deposited template layer of [10]cycloparaphenylene ([10]CPP) nanohoops on Au(111) surface we exploit the molecular shape matching between the CN and [10]CPP for the azafullerene encapsulation with nanohoops in a guest-host complexation geometry. CN⊂[10]CPP supramolecular complexes self-assemble into an extended two-dimensional hexagonal lattice yielding a high density network of stable spin-1/2 radicals.

Peripheral nerve injury induces dystonia-like movements and dysregulation in the energy metabolism: A multi-omics descriptive study in Thap1 mice.

DYT-THAP1 dystonia is a monogenetic form of dystonia, a movement disorder characterized by the involuntary co-contraction of agonistic and antagonistic muscles. The disease is caused by mutations in the THAP1 gene, although the precise mechanisms by which these mutations contribute to the pathophysiology of dystonia remain unclear. The incomplete penetrance of DYT-THAP1 dystonia, estimated at 40 to 60 %, suggests that an environmental trigger may be required for the manifestation of the disease in genetically predisposed individuals.

Genetic Diversity and Expanded Phenotypes in Dystonia: Insights from Large-Scale Exome Sequencing.

Dystonia is one of the most prevalent movement disorders, characterized by significant clinical and etiological heterogeneity. Despite considerable heritability (~25%) and the identification of several disease-linked genes, the etiology in most patients remains elusive. Moreover, understanding the correlations between clinical manifestation and genetic variants has become increasingly complex.

A framework for translational therapy development in deep brain stimulation.

Deep brain stimulation (DBS) is an established treatment for motor disorders like Parkinson's disease, but its mechanisms and effects on neurons and networks are not fully understood, limiting research-driven progress. This review presents a framework that combines neurophysiological insights and translational research to enhance DBS therapy, emphasizing biomarkers, device technology, and symptom-specific neuromodulation. It also examines the role of animal research in improving DBS, while acknowledging challenges in clinical translation.

Deep brain stimulation halts Parkinson's disease-related immune dysregulation in the brain and peripheral blood.

Immune dysregulation in the brain and periphery is thought to contribute to the detrimental neurodegeneration that occurs in Parkinson's disease (PD). Identifying mechanisms to reverse this dysregulation is key to developing disease-altering therapeutics for this currently incurable disease. Here we utilized the longitudinal data from the Parkinson's Progression Marker Initiative to demonstrate that circulating lymphocytes progressively decline in PD and can be used to predict future motor symptom progression.