Hypertension in people as young as the mid-30s can predict late-life cerebrovascular disease and brain shrinkage. Intensive reduction of blood pressure can prevent the damage, but not when given in late life.
In vicinity of plaques, astrocytes and glia change gene expression in concert.
These cells accumulate in old mouse and human hippocampi, as well as in a mouse model of neurodegenerative disease.
Changes in the composition of the cerebrospinal fluid and synapses may reveal novel insights into AD pathology.
Protein levels track with cognitive function and can distinguish Alzheimer’s patients from controls.
What’s with all those head-to-head comparison studies of academic and commercial biomarker tests? Could we not just pick one that works, and be done?
A plasma assay for Alzheimer’s could radically speed up screening for clinical trials; alas, competing assays don’t measure the same thing.
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.
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.
Plasma markers basked in the limelight at this year’s Alzheimer Association International Conference, held July 14-18 in Los Angeles. No sooner had researchers reported that mass spec and immunoassays of Aβ42/40 in plasma reproducible identify amyloid in the brain, than news of phospho-tau markers created hubbub. Scientists reported that species of phospho-tau, including p181 and p217, appear in the CSF and in the plasma of AD patients decades before dementia onset—even before they test positive on an amyloid PET scan. The findings, from several labs, pit these modifications to tau as very early responses to amyloid pathology. Together, plasma Aβ and plasma p-tau changes raise the tantalizing possibility that a simple blood test could capture the two pathological hallmarks of AD pathology decades before symptoms emerge. But maybe not so fast. A round-robin comparative study found poor agreement among 11 different plasma Aβ tests, leaving scientists scrambling to find an explanation, with some arguing for a slow and steady approach to marker development and others willing to push ahead. Read Alzforum’s six-part series, which also covers emerging markers of synaptic and cognitive dysfunction, and proteomic signatures of disease subtypes and polygenic risk.
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.
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?
New in last 7 days
Latest Comments