Old Cytokine, New Tricks? Astrocyte IL-3 Pokes Microglia in AD
Interleukin-3, produced by astrocytes in the brain, helps microglia corral amyloid plaques in Alzheimer’s.
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Genomic Double-Stranded RNA: Does C9ORF72 Cause Viral Mimetic Disease?
Typically a sign of viral infection, double-stranded RNAs were spotted in C9ORF72 carriers, in whom they mingled with cytoplasmic TDP-43 inclusions. In mice, dsRNAs spread between connected neurons, provoking Type I interferon response and killing cells.
Paper Alert: pQTLs Pin GWAS Loci to Tissue Proteins, Drug Targets
Scientists linked genetic risk variants with protein changes in Alzheimer’s brain, cerebrospinal fluid, and plasma. They identified known drugs that target some of them.
Peering Inside Stubby and Mushroom Dendritic Spines
In cultured neurons, these types of spines contain similar amounts and distributions of synaptic proteins, but mushroom spines boast more secretory and trafficking proteins, forging stronger synapses. And, holy moly, the videos!
Taming ApoE Via the LDL Receptor Calms Microglia, Slows Degeneration
In a tauopathy mouse model, overexpressing the receptor lowered ApoE, prevented microglial activation, and lessened neurodegeneration. LDLR—a drug target for neuroprotection?
Tau PET Best Predicts Short-Term Decline in Early Alzheimer’s
Compared to amyloid PET and cortical thickness, tau PET better foretold waning cognition across the Alzheimer's disease spectrum, from cognitively normal to dementia. Age, but not sex or APOE status, hastened deterioration over two years.
Next Time You Spot That Familiar Face, Thank Your Temporal Pole
When you show a monkey an image of a familiar visage, a specialized cluster of face neurons in the monkey’s temporal pole fire rapidly. Their activity could explain the split-second speed of familiar face recognition.
iSILK Tracks Growth of Mouse Plaques at Peptide Level
Using isotope labeling and mass spectrometry imaging, researchers detail how plaques first assemble with an Aβ1-42 core, expand, then subsume Aβ1-38. Plaques start in cortex, then spread to hippocampus.
Aβ 'Receptors' Retard Fibrillization, Enhancing Toxicity
By interfering with Aβ fibril growth, prion and two other cell-surface proteins may drive production of smaller, more toxic, oligomers and protofibrils.
Paper Alert: DIAN-TU Solanezumab and Gantenerumab Data Published
Though the first two trial arms were negative on cognition, gantenerumab’s strong effect on biomarkers led to an open-label extension.
COVID-19 Prompts Choroid Plexus to Ring Alarm Bell
Even without entering the brain, SARS-CoV-2 jolts the choroid plexus into signaling danger via inflammatory signals. Microglia, astrocytes, and neurons mount a response resembling that in neurodegenerative and chronic brain disorders.
Fallout Continues After Aducanumab Approval
Two weeks after the FDA gave the nod to aducanumab, the aftershocks continue to reverberate. Critics are lambasting the agency, three members of its advisory committee resigned, and the drug’s cost has ignited calls for pricing reform. Meanwhile, Alzheime
With Little Data to Go On, Clinicians Are Left To Figure Out Way Forward
Trial data for aducanumab did not answer key questions, such as how long patients should stay on drug, leaving clinicians around the world to struggle with practical and ethical issues.
How Will Aducanumab Approval Change Clinical Practice?
Physicians have a new Alzheimer’s treatment option, but most clinics are not ready to administer it. Questions remain about eligibility and insurance, to say nothing of clinician and infusion capacity.
A New Era of Alzheimer’s Treatment
Many Alzheimer’s researchers believe the aducanumab approval heralds the beginning of treatments that slow disease progression—but even they are aghast at the price and hope the drug will not sideline other trials.
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