In Alzheimer’s, we saw a failure of folate uptake via the FDH pathway, but FOLR1–folate entered via GFAP + ve astrocytes, supplying neurons directly, and this was associated with the hypermethylation of neuronal nuclei, suggesting a shutdown of function as part of the pathology in severe Alzheimer’s disease [32,33]. This evidence concerns the gene GFAP and early-onset autosomal dominant Alzheimer disease.