At this year’s AAIC, no sooner had scientists reported that phospho-tau in the CSF might reflect early responses to amyloid, than they reported parallel data for phospho-tau in blood.
At AAIC, researchers touted phospho-tau species, especially p217 and p181. They tick up in CSF as an early response to amyloid accumulation.
Using a collection of isogenic iPSC-derived neurons harboring different familial AD mutations, researchers found that, across the board, the mutations meddled with endosomes via elevated β-CTF.
The phenotype of ApoE4 astrocytes and microglia resembles that of these cells in Alzheimer’s brain. Could defects in lipid metabolism and the extracellular matrix bring on the disease?
Different polymorphisms in MS4A genes up- or downregulate levels of TREM2, modulating levels of the shed ectodomain in the cerebrospinal fluid and AD risk.
New genes linked to early and late-onset AD offer up mechanistic insight, potential targets for treatment.
Among former National Football League players who died with CTE, tau tangles, crumbling white matter, and arteriolosclerosis independently contributed to dementia.
Functional variants of AD GWAS hits found in enhancers of myeloid genes.
Alzforum encourages users to visit the Virtual Exhibit Hall, where companies showcase their newest initiatives, products, and services. We welcome F. Hoffmann-La Roche, joining our other exhibitors — Biogen, BioLegend, Dash Genomics, Inc., Abcam, BrainXell, and the Jackson Laboratory.
When studying ApoE4, most studies have looked at what it does to neurons. Now, new research suggests this major Alzheimer’s risk allele may work much of its mischief in glial cells. Human ApoE4/4 astrocytes and microglia hoard lipids while bulking up on extracellular matrix proteins and spewing out inflammatory cytokines. Lo and behold, this resembles the behavior of astrocytes and microglia in AD brain, regardless of which ApoE genotype the person had. Does this mean ApoE4 tilts the brain toward Alzheimer’s through effects on glia?
Using CRISPR to introduce a panel of different familial AD mutations into iPSC-derived neurons, researchers have generated a resource of isogenic cells that can be used to zero in on the downstream effects of disparate mutations. They will share this resource with the research community. Initial experiments with the panel confirm what years of prior research have suggested—that mutations in APP and presenilin disrupt endosomal trafficking, and that they do so primarily via b-CTF, not Ab. The study sparked intense discussion on Alzforum.
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