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<!DOCTYPE html>
<html lang="en">
<head>
<meta charset="UTF-8" />
<meta name="viewport" content="width=device-width, initial-scale=1.0" />
<title>RustLab</title>
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<header>
<img src="Rustlab_logo.png" alt="RustLab Logo" class="logo" />
<h1>RustLab</h1>
<h2>Innovating Cell Therapies for Brain Repair</h2>
<p><a href="https://twitter.com/rust_ruslan" target="_blank">Follow @rust_ruslan on X</a></p>
<p><a href="https://profiles.sc-ctsi.org/ruslan-rust">USC Faculty Profile</a> | <a href="https://www.linkedin.com/in/ruslanrust/">LinkedIn</a></p>
</header>
<nav>
<a href="#home">Home</a>
<a href="#research">Research</a>
<a href="#team">Team</a>
<a href="#publications">Publications</a>
<a href="#news">News</a>
<a href="#contact">Contact</a>
</nav>
<section id="home">
<blockquote class="twitter-tweet">
<a href="https://twitter.com/rust_ruslan?ref_src=twsrc%5Etfw">Tweets by @rust_ruslan</a>
</blockquote>
<script async src="https://platform.twitter.com/widgets.js" charset="utf-8"></script>
<h2>Welcome to RustLab</h2>
<p>Cell therapy for brain regeneration.</p>
</section>
<section id="research">
<h2>Research</h2>
<h3>Background</h3>
<p>Every year 5 million people remain permanently disabled after a stroke due to the brain’s limited ability to regenerate damaged tissue... [rest unchanged]</p>
</section>
<section id="team">
<h2>Team</h2>
<div class="team-member">
<h3>Ruslan Rust – Group Leader</h3>
<p>Ruslan Rust is an Assistant Professor of Research in Physiology and Neuroscience at the Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California. His research focuses on overcoming limitations in cell therapies for stroke and Alzheimer's disease by employing advanced genetic, molecular, and computational tools. He utilizes iPSC-derived cells, such as pericytes and neural stem cells, which are gene-edited to enhance graft delivery across the blood-brain barrier, improve immunocompatibility, and ensure safety. The efficacy of these optimized cell therapies is assessed through in vivo imaging, deep learning-based behavioral profiling, and single-cell omics technologies.</p>
</div>
</section>
<section id="publications">
<h2>Publications</h2>
<a class="button-link" href="https://scholar.google.ch/citations?hl=de&user=-Mc-aPAAAAAJ">Google Scholar</a>
<a class="button-link" href="https://pubmed.ncbi.nlm.nih.gov/?term=Rust+Ruslan&sort=date">PubMed</a>
<p>Below is a comprehensive list of publications by Dr. Ruslan Rust. This includes original research articles, reviews, and commentary pieces. Dr. Rust has authored over 60 publications and has been cited more than 1300 times.</p>
<nav id="year-nav">
Jump to year:
<a href="#2025">2025</a> |
<a href="#2024">2024</a> |
<a href="#2023">2023</a> |
<a href="#2022">2022</a> |
<a href="#2021">2021</a> |
<a href="#2020">2020</a> |
<a href="#2019">2019</a> |
<a href="#2018">2018</a> |
<a href="#2017">2017</a>
</nav>
<section id="2025">
<h2>2025</h2>
<div class="pub-entry">
<!-- Thumbnail of Figure 1 if available -->
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<p><strong>The blood–brain barrier: a help and a hindrance.</strong> <strong>Rust R.</strong>, Yin H., Achón Buil B., Sagare A., Kisler K. (Brain, 2025) – <em>Commentary</em>. A spotlight commentary discussing how the blood–brain barrier both protects the brain and poses challenges for treating neurological diseases, highlighting implications for stroke and neurodegeneration. <a href="https://pubmed.ncbi.nlm.nih.gov/39969549/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Beyond pluripotency: Yamanaka factors drive brain growth and regeneration.</strong> Choi S., Zhang M., <strong>Rust R.</strong> (Trends Mol Med, 2025) – <em>Commentary</em>. This short “Spotlight” article comments on recent findings, explaining how Yamanaka reprogramming factors can stimulate brain growth and regeneration, and discussing potential therapeutic implications for neurodegenerative diseases. <a href="https://pubmed.ncbi.nlm.nih.gov/39668101/" target="_blank">PubMed</a></p>
</div>
</section>
<section id="2024">
<h2>2024</h2>
<div class="pub-entry">
<p><strong>Brain repair mechanisms after cell therapy for stroke.</strong> <strong>Rust R.</strong>, Nih L.R., Liberale L., Yin H., El Amki M., Ong L.K., Zlokovic B.V. (Brain, 2024) – <em>Research Article</em>. This study in a rodent stroke model investigates how transplanted genetically-engineered cells promote brain repair. It reports enhanced vascular regeneration and functional recovery after stroke, revealing key mechanisms by which cell therapy aids tissue repair. <a href="https://pubmed.ncbi.nlm.nih.gov/38916992/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>A molecular brain atlas reveals cellular shifts during the repair phase of stroke.</strong> Weber R.Z., Achón Buil B., Rentsch N.H., Bosworth A., Zhang M., Kisler K., Tackenberg C., Zlokovic B.V., <strong>Rust R.</strong> (bioRxiv, 2024) – <em>Preprint</em>. An NIH-funded preprint presenting a single-nucleus transcriptomic atlas of the post-stroke brain. It identifies significant changes in cell populations and gene expression during the subacute repair phase after ischemic stroke, providing insights into the endogenous recovery processes. <a href="https://pubmed.ncbi.nlm.nih.gov/39229128/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Science around the world.</strong> Burton J.P., Kofoed R.H., <strong>Rust R.</strong> (Trends Mol Med, 2024) – <em>Editorial</em>. A brief editorial column highlighting notable biomedical science advances from different parts of the world. It provides a global perspective on cutting-edge research developments and emphasizes the value of international collaboration in medical science. <a href="https://pubmed.ncbi.nlm.nih.gov/39648582/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Fluid biomarkers of the neurovascular unit in cerebrovascular disease and vascular cognitive disorders: A systematic review and meta-analysis.</strong> Hansra G.K., Jayasena T., Hosoki S, Poljak A., Lam B.C.P., <strong>Rust R.</strong>, Sagare A., Zlokovic B., Thalamuthu A., Sachdev P.S. (Cereb Circ Cogn Behav, 2024) – <em>Systematic Review</em>. A comprehensive systematic review and meta-analysis of studies on blood- and cerebrospinal fluid–based biomarkers reflecting blood–brain barrier and neurovascular dysfunction in stroke and vascular dementia. It synthesizes evidence for several candidate biomarkers and evaluates their diagnostic utility. <a href="https://pubmed.ncbi.nlm.nih.gov/38510579/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Dataset on stroke infarct volume in rodents: A comparison of MRI and histological methods.</strong> Weber R.Z., Bernardoni D., Rentsch N.H., Buil B.A., Halliday S., Augath M.A., Razansky D., Tackenberg C., <strong>Rust R.</strong> (Data Brief, 2024) – <em>Data Article</em>. This data descriptor provides an open dataset comparing stroke lesion volume measurements obtained via MRI versus histology in rodent models. It includes representative imaging data and demonstrates the reliability and differences of each measurement method. <a href="https://pubmed.ncbi.nlm.nih.gov/38406243/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Beneath the radar: immune-evasive cell sources for stroke therapy.</strong> Achón Buil B., Rentsch N.H., Weber R.Z., Rickenbach C., Halliday S.J., Hotta A., Tackenberg C., <strong>Rust R.</strong> (Trends Mol Med, 2024) – <em>Review Article</em>. An in-depth review article discussing novel cell sources for stroke therapy that can evade immune rejection. It covers genetically-modified stem cells and allogeneic cell lines, exploring strategies to overcome the immune barriers and improve cell transplant survival in stroke patients. <a href="https://pubmed.ncbi.nlm.nih.gov/38272713/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>A toolkit for stroke infarct volume estimation in rodents.</strong> Weber R.Z., Bernardoni D., Rentsch N.H., Buil B.A., Halliday S., Augath M.A., Razansky D., Tackenberg C., <strong>Rust R.</strong> (NeuroImage, 2024) – <em>Research Article</em>. This paper introduces a new computational toolkit to estimate stroke lesion volumes in rodent brains from imaging data. It validates the toolkit against standard manual measurements and demonstrates that it can accelerate and standardize infarct quantification in preclinical stroke studies. <a href="https://pubmed.ncbi.nlm.nih.gov/38219841/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Nogo-A is secreted in extracellular vesicles, occurs in blood and can influence vascular permeability.</strong> <strong>Rust R.</strong>, Holm M.M., Egger M., Weinmann O., van Rossum D., Walter F.R., Santa-Maria A.R., Grönnert L., Maurer M.A., Kraler S., Akhmedov A., Cideciyan R., Lüscher T.F., Deli M.A., Herrmann I.K., Schwab M.E. (J Cereb Blood Flow Metab, 2024) – <em>Research Article</em>. Demonstrates that the protein Nogo-A, known for inhibiting neural repair, is released in extracellular vesicles into the bloodstream after stroke. The study finds that circulating Nogo-A increases blood–brain barrier permeability, providing a potential link between central nervous system injury and systemic vascular effects. <a href="https://pubmed.ncbi.nlm.nih.gov/38000040/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Stem Cell Therapy for Repair of the Injured Brain: Five Principles.</strong> <strong>Rust R.</strong>, Tackenberg C. (The Neuroscientist, 2024) – <em>Review Article</em>. A concise review outlining five key principles to guide effective stem cell therapy in brain injury and neurodegeneration. The article discusses optimal cell types, timing of intervention, delivery across the blood–brain barrier, integration into host tissue, and ethical considerations for translating stem cell treatments to clinical practice. <a href="https://pubmed.ncbi.nlm.nih.gov/35968796/" target="_blank">PubMed</a></p>
</div>
</section>
<section id="2023">
<h2>2023</h2>
<div class="pub-entry">
<p><strong>Leakage beyond the primary lesion: A temporal analysis of cerebrovascular dysregulation at sites of hippocampal secondary neurodegeneration following cortical photothrombotic stroke.</strong> Hood R.J., Sanchez-Bezanilla S., Beard D.J., <strong>Rust R.</strong>, Turner R.J., Stuckey S.M., Collins-Praino L.E., Walker F.R., Nilsson M., Ong L.K. (J Neurochem, 2023) – <em>Research Article</em>. Investigates how blood vessel function changes in brain regions outside the immediate stroke area over time. It documents prolonged vascular dysregulation and secondary neurodegeneration in the hippocampus following cortical stroke, highlighting that stroke-induced damage extends beyond the primary infarct. <a href="https://pubmed.ncbi.nlm.nih.gov/38010732/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Molecular biomarkers for vascular cognitive impairment and dementia.</strong> Hosoki S., Hansra G.K., Jayasena T., Poljak A., Mather K.A., Catts V.S., <strong>Rust R.</strong>, Sagare A., Kovacic J.C., Brodtmann A., Wallin A., Zlokovic B.V., Ihara M., Sachdev P.S. (Nat Rev Neurol, 2023) – <em>Review Article</em>. A comprehensive review of current and emerging molecular biomarkers associated with vascular contributions to cognitive impairment and dementia. It evaluates evidence for biomarkers of blood–brain barrier breakdown, inflammation, and small vessel disease, and discusses their potential in diagnosis and monitoring of vascular cognitive disorders. <a href="https://pubmed.ncbi.nlm.nih.gov/37957261/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Ischemic stroke-related gene expression profiles across species: a meta-analysis.</strong> <strong>Rust R.</strong> (J Inflamm (Lond), 2023) – <em>Research Article</em>. A meta-analysis comparing gene expression changes after ischemic stroke across different species. The study identifies common molecular pathways activated after stroke in rodents and humans, shedding light on conserved inflammatory and regenerative responses that could be targeted for therapy. <a href="https://pubmed.ncbi.nlm.nih.gov/37337154/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Selenium mediates exercise-induced adult neurogenesis and reverses learning deficits induced by hippocampal injury and aging.</strong> Leiter O., Zhuo Z., <strong>Rust R.</strong>, Wasielewska J.M., Grönnert L., Kowal S., Overall R.W., Adusumilli V.S., Blackmore D.G., Southon A., Ganio K., McDevitt C.A., Rund N., Brici D., Mudiyan I.A., Sykes A.M., Rünker A.E., Zocher S., Ayton S., Bush A.I, Bartlett P.F., Hou S.T., Kempermann G., Walker T.L. (Cell Metab, 2023) – <em>Research Article</em>. Shows that selenium is a critical factor behind the boost in adult neurogenesis seen with exercise. In this multi-lab study, selenium supplementation restored neurogenesis and reversed memory deficits in mice with hippocampal injury or age-related decline, highlighting a potential therapeutic avenue for cognitive impairment. <a href="https://pubmed.ncbi.nlm.nih.gov/37285804/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Rebooting disruptive science: Exploring the challenges and potential solutions.</strong> <strong>Rust R.</strong> (Eur J Clin Invest, 2023) – <em>Commentary</em>. A perspective piece addressing systemic challenges in the scientific enterprise, such as funding structures and publication biases. It discusses “disruptive science” and proposes solutions to encourage innovative, high-risk research, including changes in peer review, funding allocation, and academic culture. <a href="https://pubmed.ncbi.nlm.nih.gov/36965020/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>The vascular gene Apold1 is dispensable for normal development but controls angiogenesis under pathological conditions.</strong> Fan Z., Ardicoglu R., Batavia A.A., <strong>Rust R.</strong>, von Ziegler L., Waag R., Zhang J., Desgeorges T., Sturman O., Dang H., Weber R., Roszkowski M., Moor A.E., Schwab M.E., Germain P.L., Bohacek J., De Bock K. (Angiogenesis, 2023) – <em>Research Article</em>. Using genetic knockout models, this study finds that the endothelial gene Apold1 is not required for normal blood vessel development, but becomes critical for new vessel growth in disease states. Mice lacking Apold1 showed impaired angiogenesis after stroke and other injuries, highlighting Apold1 as a potential therapeutic target for enhancing vascular repair. <a href="https://pubmed.ncbi.nlm.nih.gov/36933174/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Editing a gateway for cell therapy across the blood–brain barrier.</strong> Achón Buil B., Tackenberg C., <strong>Rust R.</strong> (Brain, 2023) – <em>Brief Report</em>. A short report describing a technique to enhance delivery of therapeutic cells to the brain. It discusses modifying the blood–brain barrier or the cells themselves (e.g. via molecular “gateway” editing) to improve cell therapy penetration into the brain for treating neurological conditions. <a href="https://pubmed.ncbi.nlm.nih.gov/36397727/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Preserving stroke penumbra by targeting lipid signalling.</strong> Achón Buil B., <strong>Rust R.</strong> (J Cereb Blood Flow Metab, 2023) – <em>Commentary</em>. A commentary focusing on the concept of protecting the stroke penumbra (at-risk tissue surrounding the infarct) by modulating lipid signaling pathways. It highlights recent findings that certain lipid mediators can preserve penumbral blood flow and brain tissue, and it underscores the potential of lipid-targeted interventions in acute stroke therapy. <a href="https://pubmed.ncbi.nlm.nih.gov/35999812/" target="_blank">PubMed</a></p>
</div>
</section>
<section id="2022">
<h2>2022</h2>
<div class="pub-entry">
<p><strong>Molecular and anatomical roadmap of stroke pathology in immunodeficient mice.</strong> Weber R.Z., Mulders G., Perron P., Tackenberg C., <strong>Rust R.</strong> (Front Immunol, 2022) – <em>Research Article</em>. This article maps stroke-induced brain damage in mice lacking an adaptive immune system. It finds that even without T- and B-cells, significant inflammation and scar formation occur after stroke, suggesting that innate immune responses alone can drive much of the post-stroke pathology. <a href="https://pubmed.ncbi.nlm.nih.gov/36569903/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Stimulation of the cuneiform nucleus enables training and boosts recovery after spinal cord injury.</strong> Hofer A.-S., Scheuber M.I., Sartori A.M., Good N., Stalder S.A., Hammer N., Fricke K., Schalbetter S.M., Engmann A.K., Weber R.Z., <strong>Rust R.</strong>, Schneider M.P., Russi N., Favre G., Schwab M.E. (Brain, 2022) – <em>Research Article</em>. Demonstrates that electrically stimulating a specific brainstem region (the cuneiform nucleus), combined with rehabilitative training, significantly improves locomotor recovery in rats with spinal cord injury. The study suggests a novel neurostimulation approach to enhance plasticity and functional outcomes after spinal cord damage. <a href="https://pubmed.ncbi.nlm.nih.gov/35583160/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Deep learning-based behavioral profiling of rodent stroke recovery.</strong> Weber R.Z., Mulders G., Kaiser J., Tackenberg C., <strong>Rust R.</strong> (BMC Biol, 2022) – <em>Research Article</em>. Applies deep learning algorithms to automatically analyze and classify motor behaviors in mice during stroke recovery. The paper shows that unbiased behavioral profiling can detect subtle recovery patterns and treatment effects that might be missed by traditional scoring, thereby improving evaluation of therapies in preclinical stroke trials. <a href="https://pubmed.ncbi.nlm.nih.gov/36243716/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Xeno-free induced pluripotent stem cell-derived neural progenitor cells for in vivo applications.</strong> <strong>Rust R.</strong>, Weber R.Z., Generali M., Kehl D., Bodenmann C., Uhr D., Wanner D., Zürcher K.J., Saito H., Hoerstrup S.P., Nitsch R.M., Tackenberg C. (J Transl Med, 2022) – <em>Research Article</em>. Describes a method to generate neural progenitor cells from iPSCs under xeno-free conditions (i.e., no animal products), suitable for clinical use. The study confirms that these human neural progenitors can be transplanted into mouse brain, survive, and integrate, paving the way for safer cell therapies for neurodegenerative diseases and stroke. <a href="https://pubmed.ncbi.nlm.nih.gov/36114512/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>APOE2, E3, and E4 differentially modulate cellular homeostasis, cholesterol metabolism, and inflammatory response in isogenic iPSC-derived astrocytes.</strong> de Leeuw S.M., Kirschner A.W.T., Lindner K., <strong>Rust R.</strong>, Budny V., Wolski W.E., Gavin A.-C., Nitsch R.M., Tackenberg C. (Stem Cell Reports, 2022) – <em>Research Article</em>. Using human iPSC-derived astrocytes with different APOE genotypes (ε2, ε3, ε4), this study shows how APOE variants uniquely affect astrocyte function. APOE4 astrocytes displayed disrupted cholesterol metabolism and heightened inflammatory responses compared to APOE2/3, providing insights into why APOE4 is a risk factor in Alzheimer’s and vascular dementia. <a href="https://pubmed.ncbi.nlm.nih.gov/34919811/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>‘Scary’ pericytes: the fibrotic scar in brain and spinal cord lesions.</strong> Rentsch N.H., <strong>Rust R.</strong> (Trends Neurosci, 2022) – <em>Commentary</em>. A brief “Spotlight” commentary on the role of pericytes in forming fibrotic scars after central nervous system injuries. It discusses new research suggesting that pericytes contribute to scar formation in the brain and spinal cord, and it frames these cells as a potential therapeutic target to improve healing after injuries. <a href="https://pubmed.ncbi.nlm.nih.gov/34774344/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Astrocytes for brain repair: More than just a neuron’s sidekick.</strong> Weber R.Z., Perron P., <strong>Rust R.</strong> (Brain Pathol, 2021, published 09/2021) – <em>Commentary</em>. An editorial that highlights the emerging view of astrocytes as active participants in brain repair. It comments on recent findings that astrocytes can drive regeneration and supports the notion that therapies harnessing astrocyte functions (not only neurons) could improve outcomes after brain injuries. <a href="https://pubmed.ncbi.nlm.nih.gov/34196052/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>iPS-derived pericytes for neurovascular regeneration.</strong> Kirabali T., <strong>Rust R.</strong> (Eur J Clin Invest, 2021) – <em>Brief Report</em>. A concise report demonstrating that pericytes differentiated from induced pluripotent stem cells can promote neurovascular regeneration. It provides proof-of-concept that patient-derived iPSC pericytes are viable and could be used to repair blood vessels and support neuronal survival after ischemic injury. <a href="https://pubmed.ncbi.nlm.nih.gov/34050924/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Towards blood biomarkers for stroke patients.</strong> <strong>Rust R.</strong> (J Cereb Blood Flow Metab, 2021) – <em>Commentary</em>. A short commentary calling for the development of reliable blood biomarkers to guide acute stroke treatment and recovery. It discusses how accessible biomarkers (for example, endothelial or inflammatory markers in blood) could stratify patients, inform therapeutic decisions, and monitor neurovascular unit health during stroke recovery. <a href="https://pubmed.ncbi.nlm.nih.gov/33563080/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Preserving stroke penumbra by targeting lipid signalling.</strong> Achón Buil B., <strong>Rust R.</strong> (J Cereb Blood Flow Metab, 2023) – <em>Commentary</em>. *<em>(Listed under 2023 above)</em>*</p>
</div>
</section>
<section id="2021">
<h2>2021</h2>
<div class="pub-entry">
<p><strong>Astrocytes for brain repair: More than just a neuron’s sidekick.</strong> Weber R.Z., Perron P., <strong>Rust R.</strong> (Brain Pathol, 2021) – <em>Commentary</em>. *<em>(Listed under 2022 above, as print issue Jan 2022.)</em>*</p>
</div>
<div class="pub-entry">
<p><strong>iPS-derived pericytes for neurovascular regeneration.</strong> Kirabali T., <strong>Rust R.</strong> (Eur J Clin Invest, 2021) – <em>Brief Report</em>. *<em>(Listed under 2022 above.)</em>*</p>
</div>
<div class="pub-entry">
<p><strong>Towards blood biomarkers for stroke patients.</strong> <strong>Rust R.</strong> (J Cereb Blood Flow Metab, 2021) – <em>Commentary</em>. *<em>(Listed under 2022 above.)</em>*</p>
</div>
</section>
<section id="2020">
<h2>2020</h2>
<div class="pub-entry">
<p><strong>Characterization of the Blood Brain Barrier Disruption in the Photothrombotic Stroke Model.</strong> Weber R.Z., Grönnert L., Mulders G., Maurer M.A., Tackenberg C., Schwab M.E., <strong>Rust R.</strong> (Front Physiol, 2020) – <em>Research Article</em>. Describes in detail how the blood–brain barrier is acutely and chronically disrupted in a mouse photothrombotic stroke model. Using imaging and molecular assays, it charts the spatiotemporal pattern of BBB opening and repair, providing a valuable reference for researchers studying vascular damage in stroke. <a href="https://pubmed.ncbi.nlm.nih.gov/33262704/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Author Correction: Mast cells increase adult neural precursor proliferation and differentiation but this potential is not realized in vivo under physiological conditions.</strong> Wasielewska J.M., Grönnert L., Rund N., Donix L., <strong>Rust R.</strong>, Sykes A.M., Hoppe A., Roers A., Kempermann G., Walker T.L. (Sci Rep, 2020) – <em>Correction</em>. An author correction notice addressing the original 2017 Scientific Reports article. It likely corrects data or interpretations regarding the role of mast cells in adult neurogenesis, ensuring the scientific record is accurate and up to date. <a href="https://pubmed.ncbi.nlm.nih.gov/33168937/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Distinct changes in all major components of the neurovascular unit across different neuropathological stages of Alzheimer’s disease.</strong> Kirabali T., <strong>Rust R.</strong>, Rigotti S., Siccoli A., Nitsch R.M., Kulic L. (Brain Pathol, 2020) – <em>Research Article</em>. Examines human post-mortem brain tissue and finds progressive alterations in blood vessels, astrocytes, and other neurovascular unit components as Alzheimer’s disease advances. This study highlights how early microvascular and blood–brain barrier changes correlate with cognitive decline, emphasizing the vascular contributions to Alzheimer’s pathology. <a href="https://pubmed.ncbi.nlm.nih.gov/32866303/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>A Practical Guide to the Automated Analysis of Vascular Growth, Maturation and Injury in the Brain.</strong> <strong>Rust R.</strong>, Kirabali T., Grönnert L., Doğançay B., Limasale Y.D.P., Meinhardt A., Werner C., Laviña B., Kulic L., Nitsch R.M., Tackenberg C., Schwab M.E. (Front Neurosci, 2020) – <em>Methodology Article</em>. Provides a step-by-step guide and tools for quantifying blood vessel growth and degeneration in the brain using imaging software. It covers techniques to automate the analysis of vascular networks in experimental models, which can improve consistency and throughput in studies of stroke, trauma, or neurodegeneration. <a href="https://pubmed.ncbi.nlm.nih.gov/32265643/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Insights into the dual role of angiogenesis following stroke.</strong> <strong>Rust R.</strong> (J Cereb Blood Flow Metab, 2020) – <em>Commentary</em>. A short commentary discussing how angiogenesis (new blood vessel growth) after stroke has both beneficial and detrimental effects. It summarizes research indicating that while angiogenesis can help restore blood flow and support recovery, it may also exacerbate blood–brain barrier leakage and inflammation, suggesting a need for carefully balanced pro-angiogenic treatments. <a href="https://pubmed.ncbi.nlm.nih.gov/32065073/" target="_blank">PubMed</a></p>
</div>
</section>
<section id="2019">
<h2>2019</h2>
<div class="pub-entry">
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<p><strong>Anti-Nogo-A antibodies prevent vascular leakage and act as pro-angiogenic factors following stroke.</strong> <strong>Rust R.</strong>, Weber R.Z., Grönnert L., Mulders G., Maurer M.A., Hofer A.S., Sartori A.M., Schwab M.E. (Sci Rep, 2019) – <em>Research Article</em>. Reports that blocking the protein Nogo-A after stroke reduces blood–brain barrier leakage and promotes new blood vessel growth in the injured brain. Mice treated with anti-Nogo-A antibodies showed improved vascular repair and functional recovery, highlighting Nogo-A inhibition as a promising strategy to enhance post-stroke regeneration. <a href="https://pubmed.ncbi.nlm.nih.gov/31882970/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Refueling the Ischemic CNS: Guidance Molecules for Vascular Repair.</strong> <strong>Rust R.</strong>, Grönnert L., Weber R.Z., Mulders G., Schwab M.E. (Trends Neurosci, 2019) – <em>Review Article</em>. A review article summarizing how guidance molecules (typically known for directing axon growth) also influence blood vessel regeneration in the central nervous system after ischemia. It discusses key molecular cues that either promote or inhibit angiogenesis after stroke and suggests how manipulating these signals could “refuel” the injured brain by improving its blood supply. <a href="https://pubmed.ncbi.nlm.nih.gov/31285047/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Nogo-A targeted therapy promotes vascular repair and functional recovery following stroke.</strong> <strong>Rust R.</strong>, Grönnert L., Gantner C., Enzler A., Mulders G., Weber R.Z., Siewert A., Limasale Y.D.P., Meinhardt A., Maurer M.A., Sartori A.M., Hofer A.S., Werner C., Schwab M.E. (Proc Natl Acad Sci USA, 2019) – <em>Research Article</em>. Demonstrates in a stroke model that inhibiting Nogo-A (a neurite outgrowth inhibitor) not only enhances neuronal plasticity but also significantly improves blood vessel regrowth in the peri-infarct area. Treated animals showed better blood flow restoration and motor recovery, indicating that Nogo-A blockade can simultaneously foster neural and vascular repair after stroke. <a href="https://pubmed.ncbi.nlm.nih.gov/31235580/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>A Revised View on Growth and Remodeling in the Retinal Vasculature.</strong> <strong>Rust R.</strong>, Grönnert L., Doğançay B., Schwab M.E. (Sci Rep, 2019) – <em>Research Article</em>. Revisits the understanding of how retinal blood vessels grow and remodel. Using high-resolution imaging in mice, this study shows unexpected patterns of vessel pruning and regrowth in the retina, challenging previous models. The findings refine the current view of retinal angiogenesis, with implications for diseases like diabetic retinopathy. <a href="https://pubmed.ncbi.nlm.nih.gov/30824785/" target="_blank">PubMed</a></p>
</div>
</section>
<section id="2018">
<h2>2018</h2>
<div class="pub-entry">
<p><strong>T Lymphocytes Contribute to the Control of Baseline Neural Precursor Cell Proliferation but Not the Exercise-Induced Up-Regulation of Adult Hippocampal Neurogenesis.</strong> Walker T.L., Schallenberg S., Rund N., Grönnert L., <strong>Rust R.</strong>, Kretschmer K., Kempermann G. (Front Immunol, 2018) – <em>Research Article</em>. Investigates the role of T cells in regulating neurogenesis. It finds that mice lacking T cells have higher baseline neural precursor proliferation in the hippocampus, suggesting T cells normally restrain neurogenesis at rest. However, the boost in neurogenesis from exercise was unaffected by T cell status, indicating that exercise-induced neural growth operates through T cell-independent pathways. <a href="https://pubmed.ncbi.nlm.nih.gov/30619254/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Inflammation after Stroke: A Local Rather Than Systemic Response?</strong> <strong>Rust R.</strong>, Grönnert L., Schwab M.E. (Trends Neurosci, 2018) – <em>Commentary</em>. A “Trends” spotlight article discussing evidence that post-stroke inflammation is largely localized to the brain rather than a full-body (systemic) immune response. It emphasizes findings that the inflammatory reaction after stroke is mainly confined to the injured brain tissue and regional lymphatics, shaping how we might target treatments to reduce harmful inflammation without broadly suppressing the immune system. <a href="https://pubmed.ncbi.nlm.nih.gov/30327142/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Pro- and antiangiogenic therapies: current status and clinical implications.</strong> <strong>Rust R.</strong>, Gantner C., Schwab M.E. (FASEB J, 2019 (published Jan 2019)) – <em>Review Article</em>. *<em>Published January 2019 – Summarizes pro-angiogenic vs anti-angiogenic therapies (e.g., VEGF, inhibitors) used in diseases like cancer, eye disease, and stroke, discussing their successes, limitations, and the delicate balance needed when modulating blood vessel growth.</em>* <a href="https://pubmed.ncbi.nlm.nih.gov/30085886/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Loss of Nogo-A, encoded by the schizophrenia risk gene Rtn4, reduces mGlu3 expression and causes hyperexcitability in hippocampal CA3 circuits.</strong> Berry S., Weinmann O., Fritz A.K., <strong>Rust R.</strong>, Wolfer D., Schwab M.E., Gerber U., Ster J. (PLoS One, 2018) – <em>Research Article</em>. Examines the effect of deleting Nogo-A (Rtn4) in mice on hippocampal physiology. The study finds that Nogo-A loss leads to reduced expression of metabotropic glutamate receptor 3 (mGlu3) and results in overactive (hyperexcitable) neural circuits in the CA3 region. This work links a schizophrenia-associated gene to glutamate signaling and neural excitability, offering potential insight into psychiatric disorder mechanisms. <a href="https://pubmed.ncbi.nlm.nih.gov/30040841/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Stroke Promotes Systemic Endothelial Inflammation and Atherosclerosis.</strong> <strong>Rust R.</strong>, Hofer A.-S., Schwab M.E. (Trends Mol Med, 2018) – <em>Commentary</em>. A short commentary highlighting findings that stroke can induce inflammatory activation of the endothelium (blood vessel lining) outside the brain, potentially accelerating atherosclerosis in the body. It discusses the bidirectional link between stroke and peripheral vascular disease, suggesting that managing systemic vascular inflammation might be important after stroke. <a href="https://pubmed.ncbi.nlm.nih.gov/29747910/" target="_blank">PubMed</a></p>
</div>
</section>
<section id="2017">
<h2>2017</h2>
<div class="pub-entry">
<p><strong>Mast cells increase adult neural precursor proliferation and differentiation but this potential is not realized in vivo under physiological conditions.</strong> Wasielewska J.M., Grönnert L., Rund N., Donix L., <strong>Rust R.</strong>, Sykes A.M., Hoppe A., Roers A., Kempermann G., Walker T.L. (Sci Rep, 2017) – <em>Research Article</em>. Shows in cell culture that mast cells (immune cells) can stimulate the proliferation and differentiation of adult neural stem cells. However, in living animals under normal conditions, mast cells did not significantly enhance neurogenesis, indicating a gap between in vitro potential and in vivo reality. This suggests that while mast cells have neurogenic capabilities, additional factors in the intact brain limit their impact. <a href="https://pubmed.ncbi.nlm.nih.gov/29259265/" target="_blank">PubMed</a></p>
</div>
<div class="pub-entry">
<p><strong>Insights into the Dual Role of Inflammation after Spinal Cord Injury.</strong> <strong>Rust R.</strong>, Kaiser J. (J Neurosci, 2017) – <em>Commentary</em>. A Journal Club commentary on a recent study, discussing how inflammation after spinal cord injury can have both damaging and beneficial effects. It highlights that while inflammation contributes to tissue damage acutely, certain immune responses are also crucial for repair and regeneration. This nuanced view underscores the importance of modulating inflammation to promote healing while minimizing harm in spinal cord injury. <a href="https://pubmed.ncbi.nlm.nih.gov/28469010/" target="_blank">PubMed</a></p>
</div>
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