The aberrant re-entry of post-mitotic neurons into the cell cycle is an early event in AD pathology, preceding amyloid deposition...
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.
In a fly model, C9ORF72 pathology pulls TDP-43 from the nucleus, which leads to disrupted nuclear import and neurodegeneration.
Tau takes its place among the growing cadre of neurodegenerative disease proteins known to form liquid droplets. How the protein’s liquid form relates to its toxicity remains unclear.
Microglia lacking TDP-43 efficiently remove Aβ. In the process, they go a little crazy and also attack and destroy synapses.
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.
Negative findings for AVP-786 belie positive findings from a separate Phase 3 trial announced earlier this year.
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.
At a meeting in San Diego, researchers traded news about how TDP-43 gets trapped in the cytoplasm, finding both good and bad consequences of its exodus from the nucleus.
A gene involved in neurotransmitter regulation is the latest addition to the handful of genetic loci linked to amyotrophic lateral sclerosis in genomewide association studies...