In the year just past, Alzheimer’s researchers, families, and stakeholders felt renewed hope that new treatments might be within grasp. This update from the Alz Forum summarises how some of the increased funding might be spent.
Mutations in the transmembrane domain of Aβ-protein precursor cause early onset familial Alzheimer’s disease. They can increase the ratio of the amyloidogenic Aβ42 to the less-sticky Aβ40, but how exactly do these FAD mutations alter the processing of APP?
Could a person’s sex dictate how his or her brain reacts to amyloid? Stephen Ferguson, University of Ottawa Brain and Mind Institute, Canada, thinks it may. In a paper published December 15 in Science Signaling, his group reported that Aβ bound to the mGluR5 metabotropic glutamate receptor in postmortem brain tissue from men but not women.
Many people with Lewy body diseases (LBDs) such as Parkinson’s ultimately develop dementia, and many have Aβ plaques and tau tangles. Do they have two diseases at the same time, or is this combination of scourges a unique entity unto itself?