Tiny spheres full of oxygen soothe neuroinflammation and fight neurodegeneration, researchers reported at SfN. The concept may seem strange, but AD trials are on the horizon.
In mouse models of AD, one astrocyte purinergic receptor makes glia hyperactive, while another may suppress memory. Both are upregulated in the AD brain, researchers report.
Researchers at CTAD added to growing evidence that brain amyloid accumulation presages cognitive decline, although several different factors influence how fast that decline will happen in a given person.
At CTAD 2014, potential drugs for agitation, aggression, and other psychiatric symptoms of Alzheimer’s disease emerged as a prominent theme.
Scientists are finding how calcium dysregulation in mouse models of Alzheimer’s shrivels synapses and impairs neural plasticity, with effects that extend to the network level.
When provoked by Aβ, astrocytes unleash a torrent of inflammatory signals. Under it, neuronal dendrites wither and lingering synapses turn hyperactive.
Speakers at CTAD presented new treatment approaches, including a combination of two repurposed drugs that have no activity by themselves.
Roughly at its halfway point, a trial of a therapeutic Aβ antibody is over. Data aren’t out yet, but scientists suspect gantenerumab may have been dosed based on safety, too low to achieve an efficacious dose in the brain.
The seventh conference on Clinical Trials on Alzheimer’s Disease in Philadelphia last month covered everything from a sprinkling of new trial results to a new focus on tau PET imaging to a plea from former FDA honcho Rusty Katz that trialists stop obsessing over disease modification and aggressively pursue big therapeutic effects instead. Madolyn Rogers and Gabrielle Strobel close out their report on the meeting with a look at what role brain amyloid plays in AD, and a review of what new treatments may be in store for 2015.
No, not the ones found in champagne. Nanobubbles are teeny bubbles of oxygen touted to be anti-inflammatory and neuroprotective. Confused? Jessica Shugart explains it all in her story, the last in our coverage of this year's annual meeting. In our SfN series, also read about the role of purinergic receptors in Alzheimer's, how calcium flux early in disease spells trouble for network neurotransmission, and about new genes, Aβ receptors, an Aβ electrode, and a PET tracer for brain inflammation. In a three-part story Gwyneth Zakaib explored exosomes, an emerging topic in neuroscience, while Tom Fagan's report on the surprising origin of TREM2-positive cells in the brain reflects how little is known about this glial receptor and genetic risk factor for AD.
- Douglas Galasko on End of the RoAD for Gantenerumab? Roche Declares Prodromal Alzheimer’s Trial Futile
- Gregory J Brewer on Calcium Disruptions Wreak Synaptic Havoc
- Gary Gibson on Calcium Disruptions Wreak Synaptic Havoc
- Beth Stevens on NFκB-Activated Astroglial Release of Complement C3 Compromises Neuronal Morphology and Function Associated with Alzheimer's Disease.
- Ben Barres on NFκB-Activated Astroglial Release of Complement C3 Compromises Neuronal Morphology and Function Associated with Alzheimer's Disease.
- Randall Bateman on End of the RoAD for Gantenerumab? Roche Declares Prodromal Alzheimer’s Trial Futile
- Dieter Edbauer on Antisense Proline-Arginine RAN Dipeptides Linked to C9ORF72-ALS/FTD Form Toxic Nuclear Aggregates that Initiate In Vitro and In Vivo Neuronal Death.