Learning tests may prove more informative in clinical trials of early AD. A new one claims it can spot a difference in six days.
By shifting to home nursing and telemedicine, clinical researchers kept inching ahead during lockdowns.
In therapy-like paradigm, suppressing ApoE4 in astrocytes toned down tauopathy. This assuaged microglia, neurodegeneration, and revived nest-building.
Researchers used PET scans from 4,000 people to link RBFOX1 risk variants to amyloidosis. People with lower RBFOX1 expression in their brains had more amyloid and worse cognition.
Sending low-intensity, gamma frequency electric current through the brain boosted short-term memory, perhaps by increasing cholinergic transmission.
In cell culture, neurons with the strongest expression of cell-cycle proteins survived best in the presence of Aβ oligomers.
Disruption of the membraneless organelles may explain toxicity of tau aggregates.
In early stage trials, light and sound promoted neuronal communication, calmed immune cells, and slowed brain atrophy, but cognitive benefit remains unclear.
New data presented at the AD/PD conference offer the first evidence that a brain-shuttle strategy can work in people; the lecanemab and aducanumab antibody programs offer small updates.
The field is shifting from targeting tau’s tips to its mid-region, especially where tau binds microtubules. Several new candidates are in the clinic; whether the strategy will work remains to be seen.
A new trial will compare digital and blood-based biomarkers to amyloid PET scans in order to learn which ones best pick out early plaque accumulation.
Incorporation of a cryptic exon scuttles translation of UNC13A, but only in neurons lacking nuclear TDP-43. UNC13A ALS/FTD risk variants exacerbate the aberrant splicing.
Instead of chewing up and disposing of the amyloid they ingest, microglia appear to compact it, then spit it back out as dense-core plaque.
In postmortem brain, proteins involved in all manner of vesicular functions waxed or waned with increasing phases of disease, starting years prior to symptoms.
People who develop Type 2 diabetes before age 60 have more than double the dementia risk, and earlier dementia onset, than those without diabetes.