In collaboration with the Banner Alzheimer’s Institute, Eli Lilly will test the anti-amyloid immunotherapy in cognitively normal people with a high risk for AD based on plasma phospho-tau-217.
A subset of cognitively normal people died with an AD-like transcriptome, suggesting they may have been on the path to disease.
A meta-analysis of 2.8 million people estimates 119 in 100,000 develop dementia before age 64—twice the previous estimates. Prevalence increases with age and strikes men and women equally.
B cells in the brain's dura are long-term residents that respond to inflammation.
In an amyloidosis mouse, inhibiting the endosomal proton leak channel NHE6 sped up recycling of ApoE. This slashed amyloid deposition and restored synaptic plasticity.
Single-nucleus RNA sequencing detected microglia, astrocytes, and oligodendrocytes with unique gene expression in late-stage AD brain. Where DNA at transcription factor binding sites was accessible, target gene expression rose.
In carriers of the allele, cognition falters a bit earlier than in noncarriers. Brain amyloid, structure, and metabolism changed, as previously seen in sporadic and familial AD, but only some of the fluid markers did.
Interleukin-3, produced by astrocytes in the brain, helps microglia corral amyloid plaques in Alzheimer’s.
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.
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.
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!
In a tauopathy mouse model, overexpressing the receptor lowered ApoE, prevented microglial activation, and lessened neurodegeneration. LDLR—a drug target for neuroprotection?
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.
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.
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.