“iAssembloids” Probe Glial Roles in Neuron Survival
New 3D model shows how a tau kinase and Apoe4 astrocytes kill neurons through oxidative stress.
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Plaques Spur Spread of Tangles by Sending Synapses into Overdrive
Hyperconnectivity ushers tau pathology from the temporal lobe to the posterior cortex. Study could revive interest in trialing anti-convulsants with tau biomarkers as an outcome.
Another γ-Secretase Binding Partner Implicated in Aβ Production
Cell survival factor EBP1 binds the enzyme’s presenilin subunit, interfering with APP binding and lowering Aβ output. EBP1 drops with age and in AD brains.
Lactylation—a New Protein Modification That Slows Alzheimer’s?
In mice, lactylation of APP reduces amyloid deposits and slows disease progression.
Update on SORL1: Trafficking is Paramount, in Neurons and Microglia
Recent genetic and mechanistic studies on SORL1 place the endolysosomal system, in both neurons and microglia, front and center in the pathogenesis of AD.
Inhaled Xenon for AD?
In models of amyloidosis and tauopathy, the noble gas curbed inflammation and made microglia more phagocytic, resulting in fewer aggregates and healthier neurons.
New Atlas Catalogues Regulatory RNA Changes in Alzheimer’s
Survey of post-translationally modified and noncoding RNA identified more than 25,000 differences between AD and control brain.
Does the Brain Make Phospho-Tau to Fight Viruses?
In AD brain, cells ramp up expression of herpes virus proteins. In cultured neurons, these proteins boost p-tau, which then suppresses viral proteins.
Microglia Drive Neurodegeneration in Niemann-Pick Type C
In mice, eliminating the NPC1 gene from microglia recapitulated aspects of the lysosomal storage disorder.
Bile Acid: An Elixir of Youth?
In lab animals, lithocholic acid replicates life-extending benefits of caloric restriction.
One Last Round in an Open Debate: Final Exchange
Dennis Selkoe offers a closing response.
Can Human Cytomegalovirus Infections Spark Alzheimer’s Pathology?
In postmortem tissue, nearly half of AD patients had HCMV infections in the brain and gut. In cerebral organoids, HCMV triggered accumulation of Aβ and p-tau212.
Neuronal Activity Ups Mitochondrial Transcription, Rallying Energy Reserves
With age, this coupling erodes, making synapses sluggish. Rekindling it lessens synaptic deficits and memory loss in old mice.
One Last Round in an Open Debate: Attempt at Synthesis
Scott Small offers a closing argument.
… And a Response
Dennis Selkoe replies to Scott Small.
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