See what is happening
Stay up to date with everything Striatech. Online events, conferences, latest product news, interesting publications of our customers... Here you find everything in one place.
Publication
30 Aug 2025
When Brain Defenders Turn Destructive: How Microglia and T Cells Promote Age-Related Decline
As we get older, immune cells in the brain called microglia can become overactive and attract aggressive CD8+ T cells. These T cells then attack the brain’s axons’ protective layer, known as myelin, leading to its damage and a decline in brain function. Groh et al reveal the chain reaction behind these age-related brain changes and point to new opportunities for preventing or slowing down brain degeneration. The OptoDrum assay confirmed the link between axon degeneration and behavioral vision deficits.
8 Aug 2025
Meet the Striatech Team
Meet the Striatech Team!
Every company has a story and ours is shaped by the passionate individuals behind Striatech. Herewith, we introduce you to our team—the researchers, innovators, and creators driving our mission forward.
From our founders, who pioneered the OptoDrum system, to our Marketing & Sales team, who connect our technology with the research community, each member brings a unique perspective. Through this feature, we’ll share personal insights, challenges and what excites us about visual neuroscience and tech innovation.
Publication
1 Jul 2025
Validating Photoreceptor Replacement Therapy in a Severe LCA Mouse Model
Photoreceptor degeneration leads to severe vision loss in diseases like Leber congenital amaurosis (LCA). This study found that transplanting stem cell-derived human cone photoreceptors into a mouse model of LCA restored vision. The transplanted cells formed new connections with the host retina, and treated mice showed strong recovery of light responses and improved ability to track moving patterns in the OptoDrum. These results suggest cone transplantation could be a promising therapy for advanced retinal diseases.
23 May 2025
FELASA 2025: Advancing Vision Research and Animal Welfare
From June 2–5, 2025, Striatech will showcase the latest technologies for vision research at the FELASA Congress in Athens, with a special focus on animal-friendly testing methods. Discover our innovative, stress-reducing Non-Aversive Animal Platform for OptoDrum and other solutions that advance both science and animal welfare.
21 May 2025
Dedicated to Animal Welfare – New Non-Aversive Animal Platform
Striatech’s new non-aversive Animal Platform for the OptoDrum minimizes stress and promotes natural behavior—ideal for sensitive or behaviorally complex animal models. Key features include a calming transparent design, voluntary animal access via “Tunnel-Lid,” and improved handling.
Journal Club
28 Apr 2025
Journal Club: RIP1 Inhibition Protects Retinal Ganglion Cells in Preclinical Glaucoma Models
This Journal Club features innovative research by Kim et al., who revealed that inhibiting RIP1 kinase protects retinal ganglion cells in preclinical glaucoma models. Their work demonstrates that targeting necroptosis and inflammation can prevent cell loss and functional decline, directly linking genetic risk to inflammatory degeneration and highlighting RIP1 as a promising therapeutic target for neuroprotection in glaucoma.
24 Apr 2025
Supporting the Future of Vision Science: Striatech ARVO Travel Grant 2025
Striatech is proud to support emerging researchers in ophthalmology through the Striatech Travel Grant, in collaboration with the ARVO Foundation for Eye and Vision Research. This year, we are excited to recognize Manqi Pan from the Ohio State University, as a recipient of the 2025 grant.
15 Apr 2025
ARVO 2025: Visit Us at Booth #2114
Meet Striatech at ARVO 2025: Time to connect, and see all the latest improvements and features of Striatech products.
Publication
11 Mar 2025
Microglia-mediated Demyelination as a Protective Mechanism in CNS Neurodegeneration
Groh et al challenge the conventional understanding of myelin diseases by demonstrating that persistent encasement with damaged myelin can be more detrimental to axons than complete demyelination. They found that axon-al damage driven by cytotoxic T cells is less likely to progress to degeneration when axons are efficiently demyelinated by activated microglia. These findings identify harmful interactions between axons, glia, and immune cells that promote neurodegeneration, revealing potential therapeutic targets for myelin-related disorders. The OptoDrum device was utilized to assess visual acuity in mice, providing an unbiased behavioral quantification of functional decline resulting from the observed neurodegeneration.
Publication
11 Mar 2025
Exploring RIP1 Inhibition as Treatment for Glaucoma-Related Retinal Ganglion Cell Death
This study investigated the role of receptor-interacting protein 1 (RIP1) in glaucoma and explores its potential as a therapeutic target. RIP1 is a critical mediator of multiple signaling pathways that promote inflammatory responses and cell death. The researchers found that inhibiting RIP1 protects retinal ganglion cells (RGCs) in preclinical glaucoma models, improving RGC survival and preserving retinal function. Additionally, human glaucomatous retinas showed elevated levels of TNF and RIP3 mRNA, as well as increased microglia infiltration, highlighting the role of neuroinflammation in glaucoma pathogenesis. The study demonstrated that RIP1 inactivation suppresses microglial infiltration in the RGC layer following glaucomatous damage. In this study, the OptoDrum was specifically used to measure baseline visual acuity in mice before treatment and to conduct follow-up measurements just before the final experiment, allowing researchers to track changes in visual function throughout the course of the study.
Journal Club
7 Feb 2025
Journal Club: Aging and Injured Retinal Ganglion Cells Can Be Rejuvenated by Epigenetic Reprogramming
This Journal Club highlights groundbreaking work by Harvard Medical School scientist Bruce R. Ksander and his team. They were able to reverse aging in retinal ganglion cells, improving visual function after injury or in disease.