Speakers at AD/PD 2019 reported that AD risk factors mess up lipid metabolism in glial cells. In cellular models, speeding the clearance of fats lessened pathology.
The protein helps internalize neuronal interleukin receptors. It also promotes microglial phagocytosis. Does its absence worsen neuroinflammation and Aβ burden?
Using chemical cross-linkers to map contacts among amino acids, structural biologists predict that soluble tau is, in fact, a compact globule containing β-sheets poised to snap into a pathological formation.
Changes in the composition of the cerebrospinal fluid and synapses may reveal novel insights into AD pathology.
In Barcelona, data ran the gamut from a few hopeful little hints on new treatments to mixed signals on familiar players, and failed drugs thrown on the scrap heap.
Proteomics and protein-protein interaction research may yield clues to etiology, tracking, and treatment of granulin-related and other forms of FTD/ALS.