A behavioral variant of Alzheimer’s disease is not accompanied by shrinking of the frontal cortex. Rather, these patients have similar patterns of atrophy as those with typical AD.
Blocking a family of proteins called cytohesins helped clear toxic SOD1. Scientists speculate the inhibition just might do the same for other proteins linked to neurodegeneration.
New genetic methods make it possible to measure variations in DNA from one brain cell to the next, and to investigate whether these mosaic mutations contribute to disease.
Mutant SOD1 prevents immature lysosomes from traveling along the axon and from maturing, leaving the cell with no means to clear broken-down mitochondria.
Soluble APPα ramps up early in a mouse model of Fragile X Syndrome, and may promote symptoms of the disease. Blocking the peptide’s production could be a treatment strategy.