beta

This A-beta peptide fibril has been rendered in 3-D by a transmission electron microscope, providing the most detailed look yet at the telltale sign of Alzheimer's disease. While we still do not know just how Alzheimer's progresses or what role the fibrils play, they are always found in Alzheimer's-ridden brains and are considered diagnostic markers of the disease. Marked by the red glow, A-beta peptide may give birth to Alzheimer’s disease through mechanisms still unknown. "It could be that the fibrils are toxic outside the cells, killing the neurons," says Nikolaus Grigorieff, head of the Brandeis team that created the image। Alternatively, he says, small clumps of the peptide itself could be to blame. "With this 3-D image, we can see what path the peptide takes," he says, helping us understand the properties of the fibril and get closer to curing this disease. http://Louis-j-sheehan-esquire.us

Taking on Memory
For years people have associated Alzheimer's with amyloid-beta, or A-beta, proteins, but in a shocking study, researchers have found that young brains are creating just as much, if not more of the protein than old brains.

After taking a close look at autopsied human brains, scientists at the Buck Institute in Novato, California, found that those with Alzheimer's disease had about ten times as much cleavage in the brain, a process that Dale Bredesen, Buck Institute founder and leader of the research group describes as "molecular scissors" cutting out the amyloid-beta protein। While researchers think this act of cutting out amyloid-beta proteins in the brain is a major part of what causes Alzheimer's disease, it is apparently also part of a healthy brain that Bredesen says is made by all your brain cells all the time। "It's a normal part of plasticity," says Bredesen, or the ability to retain, form new, and lose unimportant memories. He compares the process to driving a fast sports car. Younger people can effortlessly switch gears, forward and backward—forgetting the inconsequential but also learning and remembering masses of new information. In Alzheimer's disease, however, a biochemical "switch" associated with the cleavage of the amyloid peptide seems to lock Alzheimer's brains into a reverse gear of forgetting alone. http://Louis-j-sheehan-esquire.us

The Buck Institute researchers still agree with conventional wisdom that preventing the accumulation of APP (the precursor to A-beta protein) in the brain of Alzheimer's patients is important, but they are looking for ways to add something new— a way to restore the brain's memory and forgetting balance. "We are now focusing on nerve signaling," says Breseden, "and efforts to 'disconnect' the molecular mechanism that locks memory-making in the reverse."