Speakers at AD/PD 2019 reported that AD risk factors mess up lipid metabolism in glial cells. In cellular models, speeding the clearance of fats lessened pathology.
Inhibiting the receptor activates microglia to mop up debris, making CD33 an attractive therapeutic target.
Scientists at AD/PD 2019 see a Goldilocks of microglial activation: Both too little and too much is bad in an injured brain. How could a therapy make it just right?
In people carrying two mutated copies of the trophic receptor, important brain structures, such as the corpus callosum, never developed.
Presented at AD/PD, the discovery by scientists in Uppsala is the first APP deletion found to cause Alzheimer’s disease. The same group found the Swedish and Arctic APP mutations.
The method purportedly distinguishes patients from controls with more than 90 percent sensitivity and specificity.
A tool of modern genetics, expression studies link GWAS hits to specific cell types, providing clues to pathogenesis. Microglia come up again and again.
After years of grunt work on next-gen sequencing and expression analysis, geneticists are finally reaping results. The new genes underscore the role of known pathways and cell types in disease.
Virtual Exhibit Hall
Alzforum encourages users to visit the Virtual Exhibit Hall, where companies showcase their newest initiatives, products, and services. We welcome Dash Genomics, Inc. and Abcam, which join our other exhibitors — Biogen, BioLegend, BrainXell, NanoString Technologies, and the Jackson Laboratory.
Held in romantically beautiful Lisbon, the 14th AD/PD conference was the biggest thus far, drawing 3,982 attendees from 73 countries, according to Abraham Fisher, its longtime lead organizer. But as the field grows, it has little to celebrate, and the mood reflected that. Trialists were appealing for patience and pointing to deepening clinical trials skills as they learn from setbacks on investigational therapies, most recently of lanabecestat, crenezumab, and aducanumab. Trials targeting tau were not yet reading out, but the medical food Souvenaid posted modestly positive results. At the other end of the bench-to-bedside spectrum, basic science is diversifying. Next-gen genetics is spilling out gene variants which, together with RNAseq, are energizing research into glial and lipid biology. Debate about the amyloid hypothesis, a fixture at AD/PD, evolved toward a focus on genetic variability in how a person’s innate immune system responds to amyloid deposition. Ab itself? Nothing special about it. It aggregates into an irritant as the brain’s ability to degrade it wanes with age. It starts things off, but other factors later dominate the disease. Or so researchers now think. Read Madolyn Rogers and Gabrielle Strobel’s coverage.
- David Hume and Clare Pridans on Life Without Microglia: Rare Cases of CSF-1R Mutations Paint a Grim Picture
- David Hansen on Closing the Book on NSAIDs for Alzheimer’s Prevention
- Colin Masters on Electrode Detects Aβ Aggregates in Alzheimer’s Plasma
- Andrea Tenner on Closing the Book on NSAIDs for Alzheimer’s Prevention
- Jürgen Götz on Could Disposing of Damaged Mitochondria Treat Alzheimer’s Disease?
- Miranda Orr on Plaques Age Glial Precursors, Stoking Inflammation
- John Breitner on Closing the Book on NSAIDs for Alzheimer’s Prevention
- G. William Rebeck on Closing the Book on NSAIDs for Alzheimer’s Prevention
- Dave Morgan on Closing the Book on NSAIDs for Alzheimer’s Prevention
- Marcia Ratner on Closing the Book on NSAIDs for Alzheimer’s Prevention
- Stefano Sensi on Results from Verubecestat APECS Trial Published
- Victor Tapias and M. Flint Beal on Could Disposing of Damaged Mitochondria Treat Alzheimer’s Disease?
- Karl Herrup on Results from Verubecestat APECS Trial Published
- Kaj Blennow on In Football Players With Possible CTE, Tau-PET Reveals Subtle Tau Deposition
- Christopher Rowe on In Football Players With Possible CTE, Tau-PET Reveals Subtle Tau Deposition
- Gil Rabinovici on In Football Players With Possible CTE, Tau-PET Reveals Subtle Tau Deposition
- Gregory Cole on Closing the Book on NSAIDs for Alzheimer’s Prevention
- Piet Eikelenboom on Closing the Book on NSAIDs for Alzheimer’s Prevention
- Gary Landreth on CD22 Suppresses Microglial Phagocytosis—A New Therapeutic Target?
- David Hondius on Do Tribes of Astrocytes Wage War on Synapses?
- Gary Landreth and Miguel Moutinho on Cut Loose, Soluble TREM2 Beckons Microglia to Mop Up Plaques