Interested in understanding how and why IDRs matter for cellular function?
@BBKrage and I took a deep dive into this question and – with excellent feedback and critiques from colleagues & our amazing editor – put together our perspective on this: https://t.co/kmaC3Zhp3R
New tools from my lab. Due to Minju Jeong's extensive efforts to validate the tools and Jun-Hyeok Choi's ingenious molecular design, we can now present additional methods to identify and modulate specific neuronal populations.
https://t.co/w7NNrZPzq3
RNA aptamer reveals nuclear TDP-43 pathology is an early aggregation event that coincides with STMN-2 cryptic splicing and precedes clinical manifestation in ALS https://t.co/b5k4zn4bwp
Happy Saturday! Every day is #hippocampus day! 🤓🔬I did this photo by combining several markers of misfolded tau protein with neuronal marker neun🟠, in an Alzheimer rhesus macaque model #neuroscience#Microscopy
What is the connection between synaptic dysfunction in #AlzheimersDisease and #Tau? PhD student Zheng Shen in collaboration with the lab of Alf Honigmann shows that Tau induces changes in the material properties of post-synaptic density #condensates https://t.co/GQaNQtxgx0.
APOE4 locks microglia in a state of homeostasis, preventing them from clearing amyloid plaque or beckoning astrocytes to help. Deleting APOE4 stirred microglia to dispose of plaques and tau tangles. @BrighamWomens@MayoClinic@hkust
https://t.co/FHdcTTgydW
An antibody mimicking the effects of the protective Christchurch ApoE variant prevents tau hyperphosphorylation in the mouse eye and brain. #Alzheimersdisease. @MassEyeAndEar https://t.co/ymikcLbF7k
At Leiden meeting, scientists report how lipids in microglia drive amyloid and tau pathology. @lipidsinbrain @wustl @vuamsterdam https://t.co/CjlrJCzhJl