People with ALS—especially those who progress fast—express myriad inflammatory genes in their blood monocytes.
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.
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.
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.
Trials enrolling people all at the same Braak stage would need fewer participants to show a drug effect, according to a new analysis.
Study of disease subtypes boosts case for NfL as predictor of rapidly progressing ALS.
Combining PET with MRI reveals near-complete overlap of tau tracer uptake with cortical atrophy and clinical features in typical and atypical AD.
NIH funds a five-year project to validate biomarkers for clinical trials.
ALS patients eliminate more p75 neurotrophin receptor than do healthy controls. P75 urine levels rise as disease worsens.
A simple blood draw may help distinguish garden-variety PD from other, less common parkinsonian disorders early in disease.
Branch out, scientists at Alzheimer’s Research UK conference say. Go after tau, glial activation, lipids, in a systematic way. Understand how these pathways connect to the amyloid hypothesis.
Convened by ARUK to learn from the antibody’s billion-dollar bust, industry and academic leaders declare insufficient CNS target engagement, say peripheral sink did not work, and brainstorm how to move forward.
Diurnal variations disappear as less Aβ42 reaches cerebrospinal fluid. Findings may improve timing of daily amyloid treatments.