Alzheimer's disease (AD) affects as much as 10% of the world population above 65 years of age but after years of research it is still not understood exactly how the disease appears and, even less, how to treat it. But work just published in The EMBO Journal opens the door to new ways for disease intervention by showing that lipids found throughout the brain can dissolve the large insoluble protein plaques characteristic of the disease, releasing their soluble protofibrillar components, and also that it is the soluble components and not the insoluble plaques that provoke neural death.

Embryonic stem cells (ESC) can both self-renew or differentiate into the many cells of the organism and it is crucial to understand the mechanism behind this capability if we want to use them in clinic. Developmental regulator genes are responsible for the activation of many ESC differentiation-pathways and, as such, they are a fundamental key to understand them. And now, research about to be published in Nature Cell Biology, reveals that these genes -always believed to be inactive in ESC before differentiation start - when apparently silent (non-active) are in fact poised, already on the first steps of gene activation only unable to go further due to the presence of repressor molecules.

Research about to published in the journal Molecular Psychiatry, resulting from a collaboration between scientists in Germany, Portugal and the UK, suggests that stress contribute directly to the development of Alzheimer’s disease (AD). According to the results now published, stress induces the production of amyloid beta (Ab) peptide – the molecule associated with the neural plaques characteristic of the disease – and also makes neurons more vulnerable to Ab toxicity. Administration of glucocorticoids (GC) - the production of which is the first physiological response to stress – was shown to have the same effect, confirming the role of stress in AD.

Research by Portuguese scientists - Ema Alves, Teresa Summavielle, Félix Carvalho and colleagues from the University of Porto and the Porto Polytechnic Institute - reveals how ecstasy can compromise the neurons in the brain by damaging their mitochondria – the structures responsible for energy production in the cell - causing the equivalent to a “power-cut” on the affected neurons. By showing how ecstasy can directly compromise such a crucial cellular process the research might help an eventual resolution of the two decade-long debate over whether or not ecstasy use is dangerous.

MDMA (the main component of ecstasy) leads to the production and accumulation of serotonin, a feel-good chemical, which is behind the pleasant effects of the drug.

Scientists have discovered a key mechanism involved in the correct separation of chromosomes during the formation of eggs and sperm.

The research shows that BubR1 - a gene recently shown to affect cell division – maintains the cohesion of paired chromosomes (until their time to divide) during the production of reproductive cells. Because BubR1 mutations can result in cells with abnormal numbers of chromosomes, the research has potential implications for human disorders resulting from loss or gain of chromosomes such as Down Syndrome, a disease caused by an extra copy of chromosome 21.

Portuguese scientists have shown that in bacteria the rate of beneficial mutations – those that increase the capacity of an organism to survive in a particular environment – is much higher than previously thought.

In the case of Escherichia coli, the bacteria studied, it is as much as 1,000 times higher than previously believed. The study also suggests that many more genes mutate during bacteria adaptation to a new environment than previously thought. Both results - a much higher rate of advantageous mutations and a bigger number of genes mutating - have important implications for studies in antibiotic resistance and also how bacteria develop the capacity to attack their host.