Activating this endogenous protective pathway mops up protein deposits in models of movement disorders. The strategy has advanced to trials.
The compound had shown promise for sharpening cognition in schizophrenia and Alzheimer’s, but now faces an uncertain future.
Macrophages and microglia lacking the gene incite inflammation.
Fed up with slow sharing mechanisms, Sage pioneers an end run around primary investigators, and participants opt to share health data with any qualified researcher worldwide.
Studies of two new mouse models find that this mutation leads to excitotoxicity, but little protein aggregation.
Using optogenetics to multiply dendritic spines, scientists recover lost memories in young mouse models of AD.
In some people, Aβ40 in the cerebrospinal fluid correlates with plaque load in the brain.
Results raise the tentative prospect that a medical food might have possible cognitive benefit early in disease.
Tracer uptake in the brain matches autopsy data. This opens up new possibilities for in vivo disease staging and longitudinal studies.
By modifying a cation channel to respond to magnetic fields, scientists can now control neural activity quickly and noninvasively.
New online venues welcome data that tend to get the cold shoulder from traditional journals. They offer open peer review and the ability to link papers. Nice try or publishing revolution?
Multiple studies link the amount and processing of this cell surface protein to inflammation and neurodegeneration, although what it does remains unclear.
Scientists wonder if the sodium channel blocker might also slow disease progression.
Scientists correlate increased appetite and sugar cravings in frontotemporal dementia patients with localized atrophy in the brain.
Healthy neurons tell astrocytes how to act. In the case of ALS, astrocyte signals spell trouble.