C9ORF72 Mice Point to Gain of Toxic Function in ALS, FTD Does C9ORF72 Repeat RNA Promote Protein Phase Transitions? RNA Regulator Locked Out of Nucleus by C9ORF72 Repeats Listen Up, Gene Silencing Strikes a Chord at RNA Meeting Stressed Out: RNA-binding ...
The ALS-linked RNA may convert free-floating proteins to liquid phase droplets.
Phenotypes vary depending on the partial or full-length nature of the C9ORF72 transgene.
Basic science inspires conference goers in Chicago.
The ALS- and FTD-linked protein condenses into liquid organelles but also tends to form hydrogels, some of which are permanent and toxic.
Snapshots from the Society for Neuroscience Annual Meeting Microglia Control Synapse Number in Multiple Disease States Might Normalizing Brain Development Help in Down’s Syndrome? Potential Parkinson’s Treatments Target α-Synuclein, Cell Replacement ...
Recent studies exemplify the burgeoning array of stem cell strategies to treat neurodegeneration, ranging from sending in supportive cells to switching out neurons.
The blood-brain barrier barred passage of antibodies in multiple mouse models of neurodegenerative disease, suggesting it holds up well in the face of disease.
Grid cells in the entorhinal cortex help with spatial navigation, and the cells’ function falters in young people at risk for AD.
Moving toward a common standard for fluid-based Alzheimer’s diagnosis in routine clinical care, an intergovernmental metrology agency has certified a way of quantifying Aβ42.
VasCog 2015—Highlights of a Conference Every so often, an intrepid reader steps forward to enlighten the community by organizing notes from a conference that few fellow Alzforum readers got to attend. This week, Donna Wilcock of the University of Kentucky ...
White-matter hyperintensities, astrocyte damage, hypoperfusion, and amyloid angiopathy draw scrutiny as factors in the complex relationship between cerebrovascular and neurodegenerative processes in dementia.
Ablating Gpr3 reduced amyloid burden and improved memory in various AD mouse models. Researchers propose using Gpr3 inhibitors to treat AD.
Fungal cells cropped up in multiple brain regions of all AD brains examined, but how they got there and what they are doing remains mysterious.
Excess Aβ42 trips up calcium homeostasis and precipitates the loss of spines thought to be important for memory.