Searching for a peripheral and quantitative biomarker, this cross-sectional study investigates an unexplored cohort of GBA1-PD compared to healthy controls (HC) and idiopathic PD (iPD) cases. We demonstrate that α-synuclein oligomers, expressed as proximity ligation assay (PLA) score in synaptic terminals of skin biopsy, distinguish both iPD and GBA1-PD from HC, whereas the increase in the synaptic density identifies GBA1-PD. These biomarkers have the potential to stratify and monitor patients in the context of new pathway-specific therapeutic options.

Imaging alpha-synuclein and iron in M83 mouse model of Parkinson's disease. Workflow included in vitro characterization of imaging probe (THK-565), in vivo epifluorescence (epiFL)-volumetric multispectral optoacoustic tomography (vMSOT) imaging, ex vivo high-field magnetic resonance imaging (MRI) and ex vivo staining validation and microscopy (image created with Biorender.com).

The figure shows tissue samples taken from three previous cases, revealing the cause of hemosiderin deposition in the central nervous system because of superficial siderosis.

Decreased microvascular levels of claudin-5 in the occipital and temporal lobe of patients with cerebral amyloid angiopathy are associated with intracerebral haemorrhage.

Anaesthesia and surgery activated astrocytic engulfment of hippocampal neuronal axon terminals in the mPFC and caused connectivity damage from dorsal hippocampus to mPFC and consequently impaired memory consolidation (created with bioRender.com).

This study presents the effect of neonatal hypoxia–ischemia on white matter development. Study was conducted with different imaging techniques on rat model of the injury, providing evidences that oligodendrocyte differentiation or maturation in hypoxic–ischemic brain is affected. Results were supported by studies on an in vitro model using primary rat oligodendrocyte progenitor cells.

Comprehensive molecular characterization of a cohort of 126 pathologically confirmed meningeal solitary fibrous tumors, including DNA methylation profiling, revealed the presence of three distinct methylation clusters: Cluster 1 (n = 38), Cluster 2 (n = 22), and Cluster 3 (n = 20). These methylation clusters were significantly associated with NAB2::STAT6 fusion breakpoints (fusion type), TERT promoter mutation status, histologic phenotype, and metastasis-free survival.

Clinical and molecular history of meningioangiomatosis.

To explore whether testing pTDP-43 aggregation in muscle tissue would assist in the diagnosis of ALS, we conducted a diagnostic study in 18 ALS patients and 54 randomly matched controls from ALS and muscular disease cohorts. Our results indicated that pTDP-43 was more prone to accumulation in ALS patients, enabling differentiation between ALS and non-ALS patients with high sensitivity and specificity. Moreover, we observed that accumulation of pTDP-43 occurred in muscle tissues prior to clinical symptoms and electromyographic lesions.

Shotgun proteomic and confirmatory immunohistochemical characterisation of post-mortem tissue showed region-specific and HLA-DRB*15 influenced alteration in extracellular matrix proteins expression between MS and controls. In particular, we shows that non-neurological controls have a perivascular-predominant expression pattern of these proteins that is disrupted in MS where instead a marked parenchymal deposition pattern is seen. Our study provides unequivocal evidence for a role of extracellular matrix proteins and the vasculature being key contributors to MS pathology within and outside the plaque area.

FAP+ pericyte-like cells drive the deposition of fibrillar extracellular matrix proteins such as collagen I and fibronectin in glioblastoma, facilitating glioma cell dissemination and activation of focal adhesion kinase.

A proposed model of thedemyelination by pathological TDP-43 in oligodendrocyte. The accumulation of truncated TDP-43 inoligodendrocyte, could interact with MyRF in the cytoplasm, preventing itsnuclear localization and affecting the expression of myelin-associated genes, therefore led to the dysfunctional demyelination in corpuscallosum.