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Previous research has incriminated three molecules in the pathogenesis of Alzheimer disease (AD): β-amyloid peptide, tau protein, and a particular form of apolipoprotein E (apoE) — apoE4. ApoE4 interacts with β-amyloid to enhance its neurotoxicity. In a new study, researchers assessed the interaction between apoE4 and tau protein.
Using mice that were genetically engineered to make large amounts of human tau protein plus human apoE4, apoE3, apoE2 or no apoE protein, researchers evaluated deposition of tau and other pathological features. The mice that produced apoE4 developed markedly more deposits of tau, greater brain atrophy, and greater brain inflammation than did mice that made apoE2 or apoE3. Mice that made no apoE protein were protect…