Senescent astrocytes spew HMGB1, a harbinger of cell death. Blocking this release prevented cell senescence, reduced neurofibrillary tangles, and improved memory in mice.
Alzforum readers might be forgiven for thinking all microglia do is act prominently, if mysteriously, in Alzheimer's pathogenesis. Not so. A recent flurry of papers shows that microglia can match themselves specifically to GABA synapses. They can ...
These changeable cells can revive plasticity in the adult brain, match themselves to GABA synapses, and strip away healthy synaptic spines in reaction to stress. What do they do in depression, PTSD?
Lowering TREM2 via antisense oligos cleared plaques in mice, while antibody fragments reduced shedding of sTREM2. Best therapeutic strategy? Still hazy.
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!