Stoelting Europe’s Post

Almost all #APOE4homozygotes exhibited #Alzheimerdisease pathology and had significantly higher levels of AD biomarkers from age 55 compared to APOE3 homozygotes. The study concludes that APOE4 homozygotes represent a genetic form of Alzheimer disease, suggesting the need for individualized prevention strategies, clinical trials and treatments. https://lnkd.in/dMSep5C6

Phosphorylated ubiquitin is like a cherry blossom petal on proteins, forming an intricate, functional structure. Phospho-ubiquitin (pUb) is a key molecular marker in the progression of neurodegenerative disorders. Recent studies have established levels of pUb as a clinical pharmacological biomarker for Parkinson's Disease (PD), important for drug discovery. LifeSensors' diverse range of phospho-ubiquitin tools, encompassing various phosphorylation sites and linkage lengths, illuminates the intricate mechanisms underlying protein degradation in PD and Alzheimer's Disease (AD). Explore our neurodegeneration arsenal, facilitating biomarker discovery, drug development, and precision medicine approaches. Learn more here: https://lnkd.in/g7RziSPM #phosphoubiquitin #neurodegeneration #drugdiscovery #ParkinsonsDisease

For neurodegenerative diseases, swift diagnostic timelines are critical. Three datasets from UCSF Memory and Aging Center discovered potential peripheral biomarkers for Frontotemporal Dementia, with positive implications for biomarkers for other neurodegenerative diseases, including Alzheimer’s.    The research suggests that certain genes show significant differential expression in individuals with a genetic variation associated with tauopathy. The discovery of these peripheral blood biomarkers increases the potential for easily collected and non-invasive diagnostic techniques, presenting a cost-effective alternative to PET imaging or cerebrospinal fluid collection.  The datasets can be requested via #ADWorkbench’s FAIR portal: https://bit.ly/4aUjFK3  

😀 Daily article sharing. Happy reading! 💥 Title: Unlocking the potential of circulating small extracellular vesicles in neurodegenerative disease through targeted biomarkers and advancements in biosensing ✍ Authors: Saqer Al Abdullah, Ivy Cocklereece, Kristen Dellinger* ⭐ Keywords: Exosomes, biosensing, Alzheimer's disease, Parkinson's disease  📃 Abstract：Neurodegenerative diseases (NDDs) gradually affect neurons impacting both their function and structure, and they afflict millions worldwide. Detecting these conditions before symptoms arise is crucial for better prognosis and duality of life, given that the disease processes often begin years earlier. Yet, reliable and affordable methods to diagnose NDDs in these stages are currently lacking. There’s a growing interest in using circulating extracellular vesicles (EVs), like small EVs (sEVs) also known as exosomes, as potential sources of markers for screening, diagnosing, and monitoring NDDs. This interest stems from evidence showing that these EVs can carry brain pathological proteins implicated in NDD pathology, and they can even traverse the blood-brain barrier. This review focuses on the creation of EVs, particularly sEVs with a size of less than 200 nanometers, methods for isolating sEVs, and recent advancements in biosensor development to detect NDD-related markers found in sEVs. Furthermore, it explores the potential of sEVs in diagnosing four major NDDs: Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and multiple system atrophy (MSA). 🔗 Full text: https://lnkd.in/ddGatbH2  #biomaterials #Exosomes #biosensing Editorial office: ebmxjournal@explorationpub.com

Neurodegenerative diseases are complex and are active areas of therapeutic research and development. Take Alzheimer’s Disease for example. Nearly 7 million people in the United States are estimated to be living with this disease, with a similar number in Europe. Research has shown a link between complement C3 and amyloid beta clearance, and elevated plasma C3 is associated with amyloid pathology. More recently, cerebrospinal fluid complement protein levels were found to correlate with degeneration and glial cell activation biomarkers in patients with Alzheimer’s Disease (Sandoval et al, 2024). At Kypha we are developing point of care multiplex complement assays that can help shine new lights on the role of complement in Alzheimer’s Disease. Find out more at https://lnkd.in/e6NvVrrm #complement #cytokines #clinicaltrials #biomarkers #immunebiomarkers #diagnostics #complementdiagnostics #cytokinediagnostics #immunemonitoring #realtimediagnostics #pointofcare #alzheimers #alzheimersdisease

🔬 A groundbreaking study by Chuan Qin et al. sheds light on the potential of CAR-T cell therapy in treating neurological autoimmune diseases like neuromyelitis optica spectrum disorder (NMOSD). Their single-cell multi-omics analysis of patients undergoing anti-BCMA CAR T cell treatment revealed fascinating insights into CAR T cell kinetics, function, and immune alterations in the central nervous system. Key findings include the identification of cytotoxic-like CD8+ CAR T cell clones as main effectors in autoimmunity, enhanced chemotaxis of CAR T cells across the blood-CSF barrier, and the suppression of neuroinflammation. Additionally, the study highlighted the distinctive features of CAR T cells in patients with NMOSD compared to those with hematological malignancies, paving the way for optimized immunotherapies for autoimmune disorders. This research not only deepens our understanding of CAR T cell therapy but also offers promising avenues for the future treatment of autoimmune diseases. Kudos to the team for their valuable contributions to advancing precision medicine! 🌟💉🧠 #Immunotherapy #AutoimmuneDiseases #PrecisionMedicine 🧪🔍✨

Population growth and aging mean that the number of people with dementia is forecast to reach almost 152.8 millionTrusted Source by 2050. There are several forms of dementia, but the most common, Alzheimer’s disease, currently accounts for up to 70%Trusted Source of cases. Monoclonal antibody treatments, such as lecanemab and donanemab, are the first disease-modifying therapies for Alzheimer’s. They clear the beta-amyloid plaquesTrusted Source that are a characteristic of Alzheimer’s, potentially delaying the cognitive symptoms. However, the treatments are expensive, and some experts are concerned that the risk of side effects may outweigh their benefits. In a new study from Texas A & M University College of Medicine, researchers have used a nasal spray to target microglia and astrocytes — cells that cause neuroinflammation (brain inflammation) — delaying the progression of Alzheimer’s disease in a mouse model By Catherine de Lange and Fact checked by Jill Seladi-Schulman Ph.D. https://lnkd.in/e2RQDkff

Plasma extracellular vesicle tau and TDP-43 as diagnostic biomarkers in FTD and ALS Biomarkers to identify diseases like frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) is vital for early diagnosis and therapeutic intervention. In a recent study, researchers found blood extracellular vesicles (EVs) with high levels of transactive response DNA-binding protein 43 (TDP-43) and 3R/4R tau ratios in a cohort of 704 patients. Both markers strongly correlated with neurodegeneration, and clinical and neuropsychological markers of disease severity, providing a promising biomarker for early diagnosis and monitoring. #sciencenewshighlights #ScienceMission https://lnkd.in/g4ug_FwD https://lnkd.in/gtEMnHdH

Although their exact role in the disease is debated, hardened clumps or "plaques" of a peptide called amyloid-β clog the brains of people with Alzheimer's disease. Many approved and in-development therapies aim to prevent or remove these plaques, but doing so safely has proven challenging. Researchers from RIKEN Center for Brain Science (CBS) in Japan believe they may have discovered an alternative approach to achieving this goal: boosting the activity of the brain's own amyloid-attacking enzyme, neprilysin. Studies have previously shown that mutations that lead to overproduction of neprilysin protect aging mice from plaque formation. Neprilysin pills or injections are not a viable option because they are not able to travel from the bloodstream to the brain. The researchers sought a way to increase production of the enzyme without tinkering with the genes and they discovered the preferred neurotransmitter for reward enhancement, dopamine. When the researchers gave mice with Alzheimer's-like disease a drug called levodopa, a precursor of dopamine often used to treat Parkinson's disease, for three months, the animals showed increased levels of neprilysin, and fewer plaques. It was found that neprilysin levels naturally decrease with age in normal mice, especially in the frontal part of the brain. This may make it a good biomarker for preclinical or at-risk diagnosis of Alzheimer's disease. The findings are promising and could potentially be explored for Alzheimer's patients. However, the authors note that levodopa can have severe side effects, so their next step is to gain a better understanding of how dopamine leads to increased neprilysin in order to find a safer way to boost the enzyme. https://lnkd.in/efE3dts9