Neural Cell Interactions with a Surgical Grade Biomaterial Using a Simulated Injury in Brain Organotypic Slices.

Tissue engineering research for neurological applications has demonstrated that biomaterial-based structural bridges present a promising approach for promoting regeneration. This is particularly relevant for penetrating traumatic brain injuries, where the clinical prognosis is typically poor, with no available regeneration-enhancing therapies. Specifically, repurposing clinically approved biomaterials offers many advantages (reduced approval time and achieving commercial scaleup for clinical applications), highlighting the need for detailed screening of potential neuromaterials.

N-terminus α-synuclein detection reveals new and more diverse aggregate morphologies in multiple system atrophy and Parkinson's disease.

Background: Parkinson's disease (PD) and multiple system atrophy (MSA) are classified as α-synucleinopathies and are primarily differentiated by their clinical phenotypes. Delineating these diseases based on their specific α-synuclein (α-Syn) proteoform pathologies is crucial for accurate antemortem biomarker diagnosis. Newly identified α-Syn pathologies in PD raise questions about whether MSA exhibits a similar diversity.

Enhanced detection of distinct honeycomb-structured neuronal SMARCC2 cytobodies in Parkinson's Disease via Cyclic Heat-Induced Epitope Retrieval (CHIER).

Antigen retrieval is crucial for immunohistochemistry, particularly in formalin-fixed paraffin-embedded brain tissue, where fixation causes extensive crosslinking that masks epitopes. Heat Induced Epitope Retrieval (HIER) reverses these crosslinks, improving access to nuclear and aggregated proteins. We introduce Cyclic Heat-Induced Epitope Retrieval (CHIER), an advanced technique that builds on HIER by incorporating repeated cycles of heating and cooling.

Identification of cell type-specific cell-penetrating peptides through in vivo phage display leveraged by next generation sequencing.

Vascular anomalies (VA) refer to abnormal blood or lymphatic vessel architecture, most often as a result of dysregulated growth. Venous malformations (VM), a subgroup of VAs, are triggered by activating mutations in the Angiopoietin/TIE2-PI3K/AKT/mTOR signaling pathway with TIE2 L914F (gene name TEK) being one of the most frequent mutations in patients with VMs. Although systemic targeting of the overactivated pathway is possible, it would be a therapeutic advantage to restrict treatment to only the affected lesions.