Nothing to Sneeze At: Viruses Raise Risk of Neurodegenerative Disease
Twelve severe viral illnesses boosted risk up to 15 years after infection.
NEWS
In Endosomes, SORL1 Dimerizes, Boosting Retromer Recycling of APP
SORL1 may form polymers that bind and stabilize the retromer, facilitating the recycling of APP and other substrates.
Not All Bad: Phosphorylated α-Synuclein Modulates Neurotransmission
p-S129syn better binds its synaptic vesicle protein partners than does plain α-synuclein.
In Nasu-Hakola Disease, DAP12-Deficient Microglia Kick Repair into Overdrive
The first study to survey the brain transcriptomes of people with NHD found microglia and astrocytes frantically repairing injury, and narrowing blood vessels.
Did Dementia Patient Care Go Downhill During the COVID Pandemic?
Data from six countries showed prescriptions for antipsychotic drugs rose in 2020, and remain high.
Droplets in the Bucket? Introducing en Masse Single-Synapse RNA-Seq
A new method reveals distinct synaptic states, some tied to amyloidosis, that were not seen in prior nuclear transcriptomic data.
No Accelerated Approval for Donanemab
The FDA turned down Eli Lilly’s application based on insufficient safety data, with fewer than 100 people on the drug for one year.
Ferried Into Brain, TREM2 Antibody Stirs Microglia
A transferrin receptor binding domain helps transport the antibody across the blood-brain barrier. In the brain, it roused microglia and boosted glucose metabolism.
SPOTLIGHT
Strings of SORL1?
SORL1 is a top AD risk gene, and the protein it encodes is responsible for whisking other proteins, including APP, out of the endosome. A new study illuminates what could be a key mechanism involved in the process. SORL1 dimerizes on the endosomal membrane, and this pairing appears critical for endosomal recycling. It may even form polymers.
Not All Bad: Phosphorylated α-Synuclein Modulates Neurotransmission
Lewy bodies accumulate α-synuclein phosphorylated at serine 129, but does this modified synuclein have a physiological function? Yes, according to two recent studies. Both claim that neural activity sparks S129 phosphorylation. One shows that this modification facilitates α-synuclein binding to synaptic vesicle proteins; the other that p-S129syn enhances neurotransmission. Mice living in an enriched environment make more p-S129syn than jaded controls and muster stronger synaptic plasticity.
Nasu-Hakola Transcriptomics
Homozygous mutations in TREM2 or its adaptor, DAP12, lead to an early onset dementia known as Nasu-Hakola disease. The first study to analyze cellular transcriptomes of people with the disease found that glia are intensely engaged in tissue repair and wound healing, while oligodendrocytes stop producing myelin, the vasculature shrinks, and neurons fade. Counterintuitively, the skew toward repair may ultimately contribute to the damage, scientists proposed.
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