Ruslan Rust

The paper uses a connectome model of the fruit-fly nervous system to simulate motor recovery after neuronal loss, finding that targeted cell replacement based on identity and connections improves recovery.

In 72,644 matched bioRxiv preprint-publication pairs, LLM-extracted primary abstract claims were unchanged or minorly revised in about 90%; hedging shifted toward caution in 8.4% versus confidence in 4.2%.

This study shows that progranulin deficiency causes microvascular and neurovascular unit changes in FTD-GRN, affecting perfusion and signaling pathways.

The paper identifies shared and disease-specific vascular signatures in Alzheimer's, frontotemporal dementia, and Huntington's disease using transcriptomic analysis of brain vessel datasets.

This study identifies molecular changes in vascular and synaptic proteomes of human temporal lobe epilepsy, revealing BBB disruption and synaptic remodeling.

This study shows that using a dual safety switch to eliminate neural grafts after stroke impairs functional recovery despite effective cell ablation.

This paper develops CAR-NSC therapy targeting integrin αvβ3 to improve spatial distribution and tissue engagement of transplanted cells in stroke models.

This study uses mouse models to show that Notch3 mutations in pericytes and smooth muscle cells cause distinct vascular and neuroinflammatory changes in CADASIL.

This study shows that disrupting the SYNGAP1 PDZ ligand motif speeds up differentiation of human iPSC-derived GABAergic neurons, revealing its role in neuronal maturation.

This study shows that hypoxic preconditioning of human iPSC-derived neural progenitor cells improves their survival and function after transplantation in a stroke mouse model.

This study shows that transplanting iPSC-derived neural progenitor cells improves long-term recovery after stroke in mice by promoting tissue repair and reducing neurological deficits.

This study investigates how different APOE genotypes affect human astrocytic energy metabolism, finding reduced ATP production in APOE4 astrocytes but increased mitochondrial respiration and glycolytic capacity.

This study creates a single-cell transcriptomic atlas of the mouse brain after stroke, revealing cell-specific molecular changes and shared features with human stroke lesions.

This study shows that iPSC-derived pericytes retain key functions under hypoxia, suggesting their potential for treating ischemic and neurodegenerative disorders.

This study shows that delayed transplantation of neural progenitor cells after stroke improves graft survival and proliferation in mice.

The paper identifies and characterizes neuro-endothelial cells (NECs) in mouse brain and kidney, showing their role in regulating blood flow and immune balance through Nos1 and Cytl1.

The paper introduces a semi-automated toolkit to estimate stroke infarct volumes in rodents using MRI and histological sections, showing high correlation between the two methods.

The paper characterizes human iPSC-derived brain pericytes, showing they closely resemble primary pericytes in protein composition and function, and demonstrate therapeutic potential in neurological disorders.

This study investigates cerebrovascular changes in the hippocampus after cortical stroke, showing sustained vascular leakage and structural remodeling beyond the primary infarct site.

This study compares gene expression profiles of stroke-affected tissue across species and time points to identify heterogeneity in stroke-related pathways and gene expression changes.

This paper develops a deep learning-based method for analyzing rodent stroke recovery using 3D gait tracking and benchmarking against conventional tests.

This paper develops xeno-free iPSC-derived NPCs compatible with GMP for clinical use, showing long-term survival and differentiation into neurons in vivo.

This study evaluates the impact of immunosuppression on stroke pathology in different mouse models, finding distinct anatomical and molecular changes that affect recovery and inflammation.

This study shows APOE alleles E2, E3, and E4 differentially affect astrocyte metabolism, cholesterol handling, and inflammation in isogenic iPSC-derived cells, with E4 showing disease-relevant dysregulation.