New Insight on Cause of Alzheimer's

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For years researchers have known that a small peptide named amyloid beta can cause neuronal cell death and Alzheimer’s disease, although the mechanism for how it works has been poorly understood. Recently, genetic evidence has demonstrated that the ability of amyloid beta to kill neurons requires a protein called “tau”; however, what it does to tau has been enigmatic.

Under normal conditions, tau is found in the long axons of neurons that serve to connect neurons with their targets, often far from the cell body itself.

“We know amyloid beta is a bad guy,” says study leader Stuart Feinstein, professor of molecular, cellular and developmental biology at Univ. of California, Santa Barbara. “Amyloid beta causes disease; amyloid beta causes Alzheimer’s. The question is how does it do it?”

Most Alzheimer’s researchers would argue that amyloid beta causes tau to become abnormally and excessively phosphorylated, says Feinstein. This means that the tau proteins get inappropriately chemically modified with phosphate groups. “Many of our proteins get phosphorylated,” adds Feinstein. “It can be done properly or improperly.”

Feinstein’s research team wanted to determine the precise details of the presumed abnormal phosphorylation of tau in order to gain a better understanding of what goes wrong. “That would provide clues for drug companies; they would have a more precise target to work on,” says Feinstein. “The more precisely they understand the biochemistry of the target, the better attack a pharmaceutical company can make on a problem.”

The team’s initial hypothesis suggesting that amyloid beta leads to extensive abnormal tau phosphorylation turned out not to be true. “We all like to get a curve ball tossed our way once in a while, right?” says Feinstein. “You like to see something different and unexpected.”

They found that when they added amyloid beta to neuronal cells, the tau in those cells did not get massively phosphorylated, as predicted. Rather, the surprising observation was the complete fragmentation of tau within one to two hours of exposure of the cells to amyloid beta. Within 24 hours, the cells were dead.

The findings are reported in the Journal of Biological Chemistry.

Research reveals how Alzheimer's spreads within the brain

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Sciencecentic.com

A research in mice has demonstrated how tangles of a so-called tau protein can spread within the brain. Tangled masses of that tau protein contribute to several neurodegenerative diseases - those that destroy brain functions - including Alzheimer's disease. The research has provided insights into how tau tangles spread that allow comparisons with the way prions, those that cause Creutzfeldt-Jakob Disease, destroy brain tissue.

Dr Michel Goedert of the Medical Research Council Laboratory of Molecular Biology in Cambridge contributed to the study alongside colleagues in Switzerland and Germany and the results are published today in the online edition of Nature Cell Biology.

Speaking about the study, Dr Goedert made it clear that it would be incorrect to suggest that Alzheimer's could be contagious: 'This research in mice does not show that tau pathology is contagious or that it can spread easily from mouse to mouse. What it has revealed is how tau tangles spread within brain tissues of individual mice. It suggests that tangles of proteins that build up in the brain to cause symptoms could have some contagious properties, within brain tissue but not between mice that haven't been injected with tissue from another mouse and certainly not between people. The work describes an experimental system that will allow scientists to study the mechanisms that underlie the transmission and spread of the tangles of tau proteins connected to the symptoms of Alzheimer's disease.'

Transgenic and wild-type mice were used in the study. Transgenic mice are genetically modified to carry specific genes. In this study the mice expressed the genes for the human versions of tau proteins.

The researchers injected brain tissue from mice modified to carry the gene for the form of human tau protein implicated in neurodegenerative disease into mice that carried the normal version of the human tau protein and therefore did not already have tangles in their brain tissue. They found that the injected material went on to create tangles of tau at the injection sites. Over time, the tau tangles then spread to neighbouring regions of the brain.

In another experiment, extract from the brains of mice with the gene for mutant-human-tau was injected into the brains of a wild-type mice. In comparison to the mice transgenic for human-tau, a smaller number of tau tangles developed where the tissue was injected and there was no evidence of the tau spreading throughout the brain.

Dr Goedert concluded: 'In contrast to prion diseases, human tauopathies like Alzheimer's are believed not....read all of how Alzheimer's spreads within the brain