On the heels of news that microglia mediate synaptic loss in Alzheimer’s, researchers report they may do the same in a subtype of FTD caused by progranulin deficiency.
Compared with previously published model lines, these animals develop more features of amyotrophic lateral sclerosis and frontotemporal dementia.
Backtracking of newly synthesized amyloid precursor protein from the Golgi to the ER facilitates APP modification and Aβ production.
C9ORF72 repeats create RNA foci and dipeptide aggregates in mice, but antisense oligonucleotides suppress them.
Two new papers rekindle acrimonious debate about exactly what “loss-of-function” means when it comes to presenilin mutations in Alzheimer’s pathogenesis.
Citing “fantastic opportunity,” FDA and EMA call for rigorous science. Agency scientists tell FTD Treatment Study Group: Explore individualized outcomes, and connect biomarkers to meaningful improvement.
Hoping for better luck in clinical trials than their Alzheimer’s colleagues had in the past decade, FTD researchers are now chasing biomarkers. It’s slim pickings so far, but neurofilament, tau PET, and MRI are showing promise.
By examining polymorphisms linked to autoimmune diseases, researchers pinned two loci to Alzheimer’s risk. Both may worsen neurofibrillary tangle pathology.
Their rap sheet keeps growing. Shortly after microglia were accused of killing off synapses in Alzheimer’s disease, new evidence indicates these immune cells may do the same in FTD caused by progranulin deficiency. Deleting the complement protein that marks synapses for destruction protected these structures in a mouse lacking progranulin. Hobbling complement also improved behavior and survival, hinting that the synaptic defect might underlie many of the problems in this type of FTD.
Forget frigid temperatures. Register for Common Mechanisms of Neurodegeneration or Microglia in the Brain, and soak up bright sunshine and hot science instead. There’s still time to submit poster abstracts for these joint conferences, to be held June 12 through 17, 2016, in Keystone, Colorado. The programs feature cutting-edge topics, from protein templating and transmission to the role of immune cells in synapse maintenance and disease.
This September, cloister yourself with meeting organizers Stefan Lichtenthaler and Robert Vassar and fellow BACE aficionados at this converted monastery near Munich for the BACE Proteases in Health and Disease conference. Graduate students and postdoctoral fellows in the United States can apply for travel scholarships to defray the cost of transcontinental travel. Register by June 15, 2016. See meeting website for more details. [Image courtesy of Kloster Seon archive.]
A growing number of studies have hinted that neurogranin may be a promising biomarker for Alzheimer’s disease. How promising? New meta-analyses by Henrik Zetterberg and Bob Olsson suggest that the synaptic protein is elevated nearly twofold in the cerebrospinal fluid of people with Alzheimer’s relative to controls. Baseline levels are also higher in people with MCI who go on to develop Alzheimer’s dementia, compared to those who do not. Plasma levels do not appear to correlate with disease. View the aggregated data and analyses in AlzBiomarker and stay tuned for further additions to the database.
- Timothy Sargeant on Microglia Prune Synapses in a Subtype of Frontotemporal Dementia
- Michael Lardelli on Pathogenic Presenilin Mutations Generate Aβ43
- Wataru Araki on Pathogenic Presenilin Mutations Generate Aβ43
- Ray Kelleher on Pathogenic Presenilin Mutations Generate Aβ43
- Jie Shen on Pathogenic Presenilin Mutations Generate Aβ43
- Maria Teresa Ferretti, M. Florencia Iulita and Sonia Do Carmo on Paper Alert: Microglia Mediate Synaptic Loss in Early Alzheimer’s Disease
- Wataru Araki on New Gene Strengthens Link Between ALS and FTD
- John Hardy on New Genetic Method Connects Immune Genes to Alzheimer’s
- Kaj Blennow on CSF Tau Rivals Aβ for Predicting Cognitive Decline
- Walter A. Rocca on Dementia Incidence in Britain Dropped, Mostly in Men
- Chengxuan Qiu on Dementia Incidence in Britain Dropped, Mostly in Men