Alzheimer’s: amyloid comes from liver
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A recent study has unexpectedly pointed to the liver as the origin of Alzheimer's plaques and not the brain, scientists from ModGene LLC and the Scripps Research Institute wrote in the Journal of Neuroscience Research. The authors say that their findings may completely change experts' idea about the disease and how to treat and prevent it.
They used laboratory mice to determine which genes influence how much amyloid builds up in the brain. Three genes were found to protect mice from amyloid build-up and deposition. A lower expression of each gene in the liver protected their brains. One of the genes encodes presenilin - a protein found on the membrane of cells which researchers believe contributes towards Alzheimer's development in humans. The team have been on a genetic search-and-find mission, concentrating on naturally occurring, inherited differences in neurological disease susceptibility in different strains of laboratory mice. They have built up extensive databases and catalogued gene activity in different tissues, as measured by mRNA build-up. These data offer up maps of trait expression that can be superimposed on maps of disease modifier genes.
Scientists at Case Western Reserve had already mapped three genes that alter the accumulation of pathological beta amyloid in the brains of a transgenic laboratory mouse model of Alzheimer's disease to large chromosomal regions. Each region has hundreds of genes. They used crosses between the B6 and D2 mice strains and studied over 500 offspring. Sutcliffe and team used those study findings and turned their own databases of gene expression to the Alzheimer's mouse model. They were seeking out variations in gene expression that correlated in Alzheimer's susceptibility between the B6 and D2 strains.
They had to create computer programs that identified each genetic variation that differentiated the B6 and D2 genomes, and then ran a regression analysis of each difference (a mathematical correlation analysis). Read more: medilexicon.com
They used laboratory mice to determine which genes influence how much amyloid builds up in the brain. Three genes were found to protect mice from amyloid build-up and deposition. A lower expression of each gene in the liver protected their brains. One of the genes encodes presenilin - a protein found on the membrane of cells which researchers believe contributes towards Alzheimer's development in humans. The team have been on a genetic search-and-find mission, concentrating on naturally occurring, inherited differences in neurological disease susceptibility in different strains of laboratory mice. They have built up extensive databases and catalogued gene activity in different tissues, as measured by mRNA build-up. These data offer up maps of trait expression that can be superimposed on maps of disease modifier genes.
Scientists at Case Western Reserve had already mapped three genes that alter the accumulation of pathological beta amyloid in the brains of a transgenic laboratory mouse model of Alzheimer's disease to large chromosomal regions. Each region has hundreds of genes. They used crosses between the B6 and D2 mice strains and studied over 500 offspring. Sutcliffe and team used those study findings and turned their own databases of gene expression to the Alzheimer's mouse model. They were seeking out variations in gene expression that correlated in Alzheimer's susceptibility between the B6 and D2 strains.
They had to create computer programs that identified each genetic variation that differentiated the B6 and D2 genomes, and then ran a regression analysis of each difference (a mathematical correlation analysis). Read more: medilexicon.com
Bioactive phenols from feverfew may boost functional drinks
Infusions of bioactive phenolic compounds from feverfew – a traditional medicinal herb – may be useful as functional ingredients, after a new study confirmed their storage stability. Read more: nutraingredients.com
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