FDA Advisory Committee Throws Cold Water on Aducanumab Filing
The panel considered the evidence for efficacy to be weak, and was troubled by too-close collaboration between the sponsor and the FDA.
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The panel considered the evidence for efficacy to be weak, and was troubled by too-close collaboration between the sponsor and the FDA.
In a mouse model of cortical multiple sclerosis, microglia and monocytes swooped in to gobble up synapses when dendritic calcium rose. Spines grew back once inflammation subsided.
Epidemiology study reveals 1.5-times higher risk of dementia after herpes virus infection. Short-term antiviral treatment appears to lower risk.
The first whole-genome manipulation of protein expression in neurons by CRISPR reveals a deadly chain of events. Bad processing by lysosomes leads to build-up of lipids and iron. Oxidative stress revs up. Neurons die by ferroptosis.
In therapy-like paradigm, suppressing ApoE4 in astrocytes toned down tauopathy. This assuaged microglia, neurodegeneration, and revived nest-building.
In animals, polyamines such as spermidine enhance autophagy, rejuvenate mitochondria, and slow cognitive decline. Buzzword: hypusination. Human data not far behind.
A set of 19 plasma proteins identified clinical Alzheimer’s cases with 97 percent accuracy, and it distinguished mild versus severe dementia. The panel was tested in two small cohorts.
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.
In an aging cohort, weak LC signal intensity on MRI correlated with plaques, tangles, and memory problems.
An unbiased “interactome” generated from human neurons could shed light on what goes wrong in tauopathies, and help identify new therapeutic targets.
In some people who had weathered COVID at home, olfactory regions in the brain shrank and executive function slowed. Will these changes resolve or persist?
In a game changer for the field, three papers report similar structures for TMEM106b fibrils. One claims they comprise the lion’s share of TDP-43 aggregates.
In a clever bit of sleuthing, Karen Ashe and colleagues appear to have solved the case of the mysterious...
Filaments of Aβ42 struck different poses in people with sporadic versus familial AD. The familial AD structure was also found in people with other neurodegenerative diseases, and even in APP knock-in mice.
These axonal swellings block action potentials, weakening neural networks in mice. PLD3, an Alzheimer’s disease risk gene, may be involved.
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