Scientists have found.

But when the proper execution of the gene that puts people at risk, ApoE4, is involved, VLDLR nearly alone is responsible for hauling the amyloid-beta away. This means that the amyloid-beta isn’t removed as quickly as it otherwise would, potentially offering it a chance to accumulate, like we find in the brains of individuals with Alzheimer’s disease. Consequently, in mice with the better versions of the ApoE protein, ApoE2 and ApoE3, amyloid is usually cleared out of the brain at a rate about twice or three times as fast since it can be in mice with the ApoE4 protein. Amyloid deposits accumulate in the brains of mice with the ApoE4 protein in much higher amounts, about 10 to 15 times just as much as in the brains of mice with either ApoE3 or ApoE2.The results claim that it may be better to prevent Abeta deposition than to improve Abeta once deposited. This method may be an effective strategy to prevent amyloid deposition before the onset of Alzheimer’s disease, but may have limited benefit in a therapeutic placing where amyloid deposits are already well set up within the brain.

Antimicrobial sutures reduce infections in human brain shunt surgery Kids born with hydrocephalus, or ‘water on the brain’ must have shunts implanted to drain the liquid from the brain to reduce harmful pressure.