Tau antibodies in the blood bind and stabilize tau as it leaves the brain, offering researchers a readout of soluble tau levels in the CNS.
TIMP2 and possibly other human plasma proteins reinvigorate aged hippocampi in mice.
The receptor responds to brain insults such as oligomeric Aβ and cellular debris by jolting microglia into clean-up mode, according to researchers at AD/PD 2017.
In tauopathy mice, ApoE4 hastened neuroinflammation and neurodegeneration. No amyloid involved. (Tip: Think A1 astrocytes.)
In the field’s march toward automated testing, scientists for the first time used biomarker cutoffs determined in one cohort to predict amyloid accumulation in a second. It worked.
Next-Generation Tau PET Tracers Strut Their Stuff Are CSF Assays Finally Ready for Prime Time? ApoE and Tau: Unholy Alliance Spawns Neurodegeneration New Evidence Confirms TREM2 Binds Aβ, Drives Protective Response Location, Conformation, Decoration: Tau ...
Prospective study links cardiovascular risk factors to brain amyloid.
Emerging data on new tau ligands raise hope of more signal, less noise, and help with a broad range of tauopathies. Read news culled from the AD/PD and HAI 2017 meetings.
By virtue of its heavy hydrogen, deutetrabenazine resists metabolism by liver enzymes, allowing clinicians to better titrate the drug.
People who developed epilepsy as children were more likely to have amyloid in their brains 50 years later, especially if they carried the ApoE4 allele.
Although shorter tau peptides formed fibrils in a dish, the R3 domain of tau seeded aggregation in cells.
Antibodies against tau lower APP expression and degrade Aβ plaques in transgenic mice.
Unlikely a disease marker, poly glycine-proline might track therapeutic efficacy in clinical trials.
The largest study yet on neurofilament light chain suggests plasma levels rise with disease and correlate with other signs of neurodegeneration.
Unbiased screen turns up genes expressed in immune cells, both inside and outside the CNS.