An astrocytic Aβ protease, destabilization of γ-secretase by FAD mutations, and an sAPP receptor all made their debuts at Heidelberg conference.
Run-on repeats not only break DNA, they thwart the crucial repair pathways needed to sew the strands back together.
Knockout mice suggest opposing effects on lysosomal enzymes and neurodegeneration in frontotemporal dementia, implicating an ATPase.
Analysis of brain tissue from Alzheimer’s patients offers a glimpse of proteomic changes in the disease.
Researchers identified nuclear protein SRSF1 as the culprit that allows aberrant C9ORF72 RNA to escape into cytoplasm and give rise to toxic dipeptide repeat proteins.
Tau takes its place among the growing cadre of neurodegenerative disease proteins known to form liquid droplets. How the protein’s liquid form relates to its toxicity remains unclear.
Transcriptional profiling of human microglia sheds light on species differences, raising caution about translatability of rodent studies.
At a conference in Heidelberg, researchers proposed that Aβ oligomers trigger local translation of tau in cytosol and dendrites, and that targeting this aberrant tau may preserve synapses.
From June 14 to 17, EMBO/EMBL hosted their second Mechanisms of Neurodegeneration symposium in Heidelberg, Germany. This open conference is rapidly becoming the place to present and debate new data on the underlying mechanisms of all neurodegenerative diseases. Read the latest on APP processing, APP receptors, tau synthesis and degradation. Find the cutting edge on the role of microglia in protecting and exacerbating disease, and the promise of human proteomics for tracking disease progression at a systems level.
Genetics isn’t just for geneticists anymore. With the rise of direct-to-consumer genetic testing companies like 23andMe, anyone can riffle through their genotypes at hundreds of thousands of positions across their genome. These include dozens of autosomal-dominant mutations for Alzheimer’s and other neurodegenerative diseases, as well as many risk alleles. Much of the data shared with customers has not been validated. Some researchers question the ethics of this data dump, while some see it as an opportunity to usher carriers of pathogenic mutations toward prevention trials.
- Sherif El-Khamisy on C9ORF72 Throws a Wrench into DNA Repair Machinery
- Li-Huei Tsai on C9ORF72 Throws a Wrench into DNA Repair Machinery
- Benjamin Wolozin on Tau Hooks Up with RNA to Form Droplets
- Shane Liddelow on Human and Mouse Microglia Look Alike, but Age Differently
- Joseph Arboleda-Velasquez on Immunotherapy for Cerebral Small Vessel Disease?
- Gabrielle Leblanc on Immunotherapy for Cerebral Small Vessel Disease?
- Elena Galea on For Better and Worse, TDP-43 Controls Microglia’s Phagocytic Prowess
- Axel Montagne, Zhen Zhao and Berislav Zlokovic on Immunotherapy for Cerebral Small Vessel Disease?
- Walter Kukull on New Study Disputes Claim That Heartburn Meds Raise Dementia Risk
- Gael Nicolas and Anne Rovelet-Lecrux on Novel presenilin mutations within Moroccan patients with Early-Onset Alzheimer's Disease.
- Matteo Santoro and Gernot Riedel on Trigger Warning: α-Synuclein Sets Off T Cells in Parkinson’s
- Markus Zweckstetter on Tau Filaments from the Alzheimer’s Brain Revealed at Atomic Resolution
- Eckhard Mandelkow on Tau Filaments from the Alzheimer’s Brain Revealed at Atomic Resolution
- David Sanders on Tau Filaments from the Alzheimer’s Brain Revealed at Atomic Resolution
- Carol Brayne and Suvi Hokkanen on For Better and Worse, TDP-43 Controls Microglia’s Phagocytic Prowess
- Christos Proukakis on Could Genetic Mosaicism in Adult Neurons Precipitate Disease?
- Richard Caselli on APOE4 Subtly Alters Brain Network Activity With Age
- Amy Borenstein on Preventing Dementia: Getting Closer to Recommendations
- Steffen Rossner on New Alzheimer’s Drug Shows Safety, Hints of Efficacy in Phase 2
- Mychael Lourenco on Loss of Tau Function Triggers Insulin Resistance in the Brain
- Michael Zasloff on Put ’Em Up: Does α-Synuclein Help Fight Microbes in the Gut?