Brains of Alzheimer’s patients contain Aβ dimers consisting of monomers Aβ37 to Aβ42 and held together by covalent bonds.
At SfN, some scientists described how circulating immune cells deliver aging to the mouse hippocampus; others held off parkinsonism by blocking the effects of eotaxin’s rise in blood. Human trials are starting.
Recent conferences revealed that tau is most toxic in oligomeric form, that tau oligomers propagate throughout the brain, and that tau oligomers might harm synapses from within or via astrocytes.
At SfN and in new papers, scientists describe how synapses crater under the combined onslaught of Aβ and tau. They also link gene-expression signatures to the selective vulnerability of excitatory neurons to tau pathology.
Disrupting circadian clocks in astrocytes and microglia unleashed harmful responses in these glial cells, leading to neuronal damage.