Researchers have published RNA expression and processing data for the cerebellum and frontal cortex, and find that C9ORF72-based ALS and sporadic disease differ greatly.
Patients and charities hope people will want to cool off again this summer.
A year after social media campaign, what happened with the money?
A new mass spectrometry analysis provides the most thorough catalog yet of modifications to tau.
Findings suggest a severe blow to the head twists the protein's backbone, which may lead to neurofibrillary tangles.
Clever optical corrections reveal microglia and neurons through the intact mouse cranium.
A C-terminal fragment of APP recruits the protein APPL1 to endosomes, causing the enlarged, overactive vesicles seen early in Alzheimer’s disease.
The foundation recognizes the two researchers for their work on the molecular underpinnings Alzheimer’s disease.
Last year's ice bucket challenge for amyotrophic lateral sclerosis netted $220 million in donations for ALS charities, and the 2015 challenge is off to a strong start with $100,000 from Major League Baseball. Alzforum looks at how all that money is being spent, on both clinical and basic research as well as patient care.
Researchers have used mass spectrometry to catalog and quantify five types of tau modification in wild-type and transgenic mouse models of AD. While their results suggest little if any difference between normal and plaque-ridden mice, they do reveal previously unknown modifications, and may provide new clues to the protein’s normal function. Other scientists praised the rigor and breadth of the work and its importance for future research. Read the story and extensive commentary.
Using an optical gadget that can be fitted to any two-photon microscope, researchers have been able to look through the skull into the mouse brain. They used a specialized mirror to straighten wayward light rays scattered by the cranium and see shape-shifting microglia and tiny dendritic spines. While the imaging technique does not probe quite as deep as light shone through a cranial window or through a thinned skull, it allows researchers to glimpse the brain’s business without disrupting it.
Neurons in Alzheimer’s disease patients accumulate swollen, dysfunctional endosomes. A new report now directly links the β C-terminal fragment of APP to this pathology. The fragment recruits a protein that keeps endosomes active, causing accelerated endocytosis and potentially stressing protein degradation pathways.
- Robert C. Green on Divvying Up the Ice Bucket Dollars: Looking Long Term
- Xue Zhang on Mutant Presenilin Knock-in Mice Mimic Knockouts, Stir Old Debate
- Sami Barmada on Scientists Eager to Test ALS Gene Therapy
- Junying Yuan on Bioinformatics Identifies Eight Master Regulators of ALS Neurodegeneration
- Eckhard Mandelkow and Yipeng Wang on Inventory of Tau Modifications Hints at Undiscovered Functions
- Daryl Bosco on Enhanced Autophagy Protects Against ALS Proteotoxicity
- Lawrence Rajendran on Partners in Crime: APP Fragment and Endosomal Protein Impair Endocytosis