A new PET tracer. Plasma glial fibrillary acidic protein. Two new, promising surrogates for astrogliosis are filling in the Alzheimer’s biomarker toolbox. Both reflect Aβ amyloid better than they do tau tangles.
As FTD consortia chase biomarkers, they see plasma NfL and neuronal pentraxin-2—which reflect neurodegeneration—change before symptoms. Trials nudge progranulin and poly-DP. Still needed: more markers of the pathophysiology that unfolds in the brain.
The first ultrasensitive plasma test for this old marker differentiates Alzheimer’s from healthy controls and non-AD dementias. It segregates people stepwise at phases of pathogenesis down to Braak stages 1 and 2 and below amyloid PET positivity.
Some people with severe COVID-19 have neurovascular injury and elevated markers of neural damage in their blood and CSF. What’s going on in their brains?
In mice, forebrain neurons with hobbled retromers ooze fragments of tau and several BACE1 substrates into the CSF. Similar proteins are up in CSF from people with MCI and Alzheimer’s disease.
Regulators in the U.S. and Europe have certified a mass-spectrometry-based blood test for amyloid-β. Plasma phospho-tau markers are poised to come next.
Two papers report that skin samples from people with Parkinson’s disease contain α-synuclein seeds that can be robustly amplified, paving the way for a reliable test for the disease.
Carriers accumulate fewer tangles than noncarriers for a given amount of amyloid, explaining how the gene variant may lower a person’s Alzheimer’s risk.
New synaptic profiling and imaging techniques are enabling scientists to zero in on synaptic proteins, including phospho-tau, that make the difference between clinical Alzheimer’s and resilience.
A slight drop in hospital admissions after amyloid PET, especially in people with positive scans, fell well short of the prespecified endpoint. Still, IDEAS is broadening into a research platform, and IDEAS 2 will add racial diversity.