Weill Cornell Medicine Enterprise Innovation’s Post

Discover the groundbreaking research of Alzheimer's Therapeutic Research Institute (ATRI)'s Neuroscience Translational Research Division (NTRD). Learn how scientists are collaborating to uncover early Alzheimer's diagnosis methods, increase clinical trial representation, and develop innovative therapies. Learn more: atri.usc.edu/ntrd/

Researchers Nicholas Sweeney, Tae Yeon Kim, Cody Morrison, et al. have found that #TraumaticBrainInjury (#TBI) increases the risk of #AlzheimersDisease by disrupting protein clearance, leading to the accumulation of toxic tau proteins in the brain. They discovered that TBI downregulates BAG3, a protein crucial for clearing damaged proteins, which contributes to #Alzheimers-related tau buildup. Overexpression of BAG3 in mouse models reduced tau accumulation and improved cognitive function, suggesting a potential therapeutic target. These findings provide new insight into the biological link between TBI and Alzheimer’s, opening avenues for developing therapies that could reduce Alzheimer’s risk after TBI. Learn More in Acta Neuropathologica | Pathology and Mechanisms of Neurological Disease https://lnkd.in/dsFAiXp9 Neuronal BAG3 attenuates tau hyperphosphorylation, synaptic dysfunction, and cognitive deficits induced by traumatic brain injury via the regulation of autophagy‑lysosome pathway - Nicholas Sweeney, Tae Yeon Kim, Cody Morrison, Gail VW Johnson, HONGJUN (Harry) FU, et al. The Ohio State University The Ohio State University College of Medicine WVU Rockefeller Neuroscience Institute Banner Sun Health Research Institute RIKEN Center for Brain Science Nagoya City University University of Rochester

One of the challenges for #DrugDiscovery for new therapies to treat neurological conditions has been the need for better models of the various cells within the human brain and the interaction between different cell types. Charles River Laboratories, in partnership with bit.bio, has gained access to a scalable and consistent supply of induced pluripotent stem cell-derived human brain cells. This enables the development of multi-cell cultures that can model neurological diseases more effectively. Malika Bsibsi, research leader at Charles River Laboratories, discussed with us the challenges of developing treatments for neurological diseases, the limitations of animal models and single-cell cultures, and how this new method could enhance drug discovery in this challenging therapeutic area. 🔈Listen here: https://lnkd.in/g2ibkDG4 #biotech #lifescience #nuerologicaldiseases #science #healthcare

Researchers in the US have delivered human neurons, that are damaged in Parkinson’s, into monkeys as a new approach for treating the condition, with the first trials set to start in patients. A team led by the University of Wisconsin-Madison and Aspen Neuroscience, Inc. developed an approach to replace lost dopaminergic neurons by first growing them from human stem cells, before transplanting them into the brains of monkeys. Five of the six monkeys in the study retained the human neurons after a week, and a higher number of the neurons were observed after 30 days, indicating that the transplants were successful in helping to replace dopaminergic neurons. Read more: https://lnkd.in/gmayHJjX #AnimalResearch #ParkinsonsDisease #ParkinsonsResearch #BrainResearch #MonkeyReseach #NHP

🎓 Recognizing Excellence in Neuroscience Research! 🧠 A standing ovation to the team at John Hopkins University for their paper "Development of a novel glucose-dendrimer based therapeutic targeting hyperexcitable neurons in neurological disorders." This study represents a significant stride forward in our understanding and treatment of neurological conditions like epilepsy and traumatic brain injury. 🔍 Summary & Key Findings: The team's pioneering work centers on the development of a generation-two glucose-dendrimer (GD2), primarily composed of glucose and ethylene glycol building blocks, to selectively target hyperexcitable neurons. Through comprehensive experimentation in primary cultures, ex vivo acute brain slices, and in vivo mouse models of acute seizures, they demonstrated the extraordinary ability of GD2 to specifically target hyperexcitable neurons, even upon intranasal delivery. This targeted approach shows potential for precise protection and restoration of neuronal function, laying the foundation for neuron-specific therapies in neurological disorders. 🌐 Explore the paper here: https://lnkd.in/g_fvdTes 🌟 Acknowledging BroadPharm's Contribution: BroadPharm’s Azido-PEG4-alcohol played a crucial role in synthesizing the novel glucose dendrimer (GD2) platform. This platform exploits the increased glucose demand and uptake of hyperexcitable neurons to specifically target and deliver anti-epileptic drugs without providing metabolizable glucose. Explore BroadPharm's spectrum of linker solutions tailored for research and development to foster further innovation: 🔗 Azido-PEG4-alcohol —>  https://lnkd.in/g8_gEXJb  🔗 More linkers —> https://lnkd.in/gVK9jp3S #Neuroscience #Epilepsy #Dendrimer #Conjugation #PEG #PEGylation #PEGLinker #PEGreagent #BioConjugationLinker #MaleimideLinker #PROTACLinker #ClickChemistryLinker

🔬 Dr. Morten Scott’s research team from Lundbeck used the COMET™ platform in preclinical model to investigate neuroinflammation, a complex biological process contributing to neurodegenerative diseases. ⬇️ Take a look at the staining images below, showcasing how the spatial profiling of mouse FFPE brain and spinal cord samples can unlock new knowledge and pave the way for discoveries in understanding these conditions. 📰 Discover how other researchers are leveraging COMET™ in neuroscience studies: https://lnkd.in/eNJ2cHqP #spatialbiology

🧠 A Major Breakthrough in Alzheimer’s Research 🚀 The Allen Institute just released an incredible study that traces the progression of Alzheimer’s at the molecular level—essentially mapping out the disease’s “pathological clock.” This research is a huge step forward in understanding how Alzheimer’s takes hold in the brain, and it brings real hope for earlier detection and better treatments. Some key findings that really stood out: 🔹 Scientists discovered molecular changes that happen years before symptoms start, which could open the door to earlier intervention. 🔹 They were able to pinpoint the exact timing of protein changes, offering a clearer picture of how the disease progresses. 🔹 This could help us develop therapies that target Alzheimer’s at its earliest stages, potentially slowing or even stopping the disease. Check out the full article here: https://lnkd.in/gKHfHAF7 #AlzheimersResearch #Neuroscience #BrainHealth #MedicalBreakthrough #AllenInstitute

In case you missed it, #Alchemab was featured in Drug Discovery World’s insightful report: 'Neuroscience: Advances in research and opportunities ahead', highlighting our 'patient-centric approach'! 💡 📰 Download the free report to read more about our unique approach to #drugdiscovery and our program, ATLX-1088, a CD33 inhibitor which 'offers a promising and novel therapeutic approach for the treatment of Alzheimer's disease'. https://lnkd.in/eCEEdBCu #biotech #lifesciences #antibodies #neuroscience #alzheimers

Another cool finding from our study, IMO, is that our model, based on early brain activity changes linked to protein buildup in symptom-free participants, forecasted brain activity changes in advanced cases retrieved from independent validation data. This finding and the other observations from our study are explained in lay terms in my blog post👇 https://lnkd.in/eikkQCw6

Recent studies reveal that amyloid beta production is not unique to neurons; it’s a byproduct of many cell types. Plaque formation, however, depends on the cellular environment’s density, which is why we primarily observe these plaques in the brain. In 3D cellular cultures using Matrigel to simulate different organ environments, this phenomenon becomes evident. While this research provides intriguing insights, I believe it could be a step backward in our understanding of Alzheimer’s. Despite significant advances like lecanemab, which targets and clears amyloid plaques, we see that Alzheimer’s progression persists. This suggests that the amyloid hypothesis alone may not fully explain the disease’s complexity. We must broaden our focus beyond plaques to address the multifaceted nature of Alzheimer’s.