According to new research, as both mice and humans grow older, immune signals change at the interface between blood and cerebrospinal fluid.
Perfectly healthy mitochondria can sicken neurons simply by being in the wrong place.
A man lacking ApoE appears to have no cognitive deficits, and his brain and CSF biomarker profiles appear normal. Some claim the findings support ApoE as a rational drug target for AD.
The first large-scale surveys of DNA methylation in Alzheimer’s brains turned up numerous altered regions that may point to new genes involved in pathology.
Researchers predict that a new BACE1 mouse recapitulates the early stages of sporadic Alzheimer’s, and can serve as a testing ground for BACE1 inhibitors.