Lysosomal Protein TMEM106b Is Tightly Linked to TDP-43, Tau Pathology
In mouse models of ALS and tauopathy, neurons with TMEM106B aggregates, but not those without, lost nuclear TDP-43 or accumulated p-tau, respectively.
6500 RESULTS
Sort By:
In mouse models of ALS and tauopathy, neurons with TMEM106B aggregates, but not those without, lost nuclear TDP-43 or accumulated p-tau, respectively.
ApoE aggregates are central to Aβ plaque formation. The fateful pairing may happen in microglial lysosomes, where ApoE forms fibrillar aggregates.
In certain regions of the brain, microglia internalize proteins from the plasma. At least one of these peripheral proteins—ApoA-I—supports microglial phagocytosis.
Combining isotopic labeling and transcriptomics, scientists found that mature plaques in mice wreaked more havoc on surrounding synapses than immature ones.
Glia need exactly the right amount of tau for lipid droplets to bud from the endoplasmic reticulum. The droplets soak up toxic lipids spilled by stressed neurons.
In a head-to-head comparison with aducanumab, gantenerumab, and donanemab, lecanemab had the highest affinity, especially for smaller aggregates.
In two hospital systems, people who received heparin were diagnosed with AD a year later than people who never took the anticoagulant.
The NIH removed Masliah from his post after an investigation found two publications with falsified data. At least 130 more papers with 500 co-authors face allegations.
The analysis of nearly 8,000 brains turned up three genes linked to cerebrovascular disease, and one linked to tangles.
A whole-genome sequencing study estimated that people are two to three times more likely to be affected by these mutations than predicted by epidemiology.
In mice with prion disease, microglia shifted from gobbling up misfolded protein to engulfing flagging neurons. This change coincided with symptom onset.
Scientists are honing transferrin receptors to whisk bulky, anti-Aβ antibodies throughout the brain without setting off ARIA and anemia. By halving the effector function of their antibody transport vehicle, Denali researchers blunted red blood cell loss a
The adaptive nature of the interface between blood and brain led some scientists to envision it more like an actively managed border crossing, not a wall.
With genetic tinkering to their antibody transport vehicle, Denali scientists aim to temper both ARIA and anemia, while maintaining potency against Aβ.
Brain regions that have most recently evolved may be most vulnerable to FTLD.