A New Cause For Mental Disease


R.I.P Portuguese Science


Schistosomiasis- New Urine Test Could Help Millions


When Bad News Is Good News For Neurodegenerative Diseases


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Scientists have just identified several molecules capable of reversing the brain abnormalities of Parkinson’s disease (PD), while also uncovering new clues for its origin in a study just published in the journal Disease Models and Mechanisms (1). PD is characterised by abnormal deposits of a brain protein called alpha-synuclein throughout the damaged brain regions, but exactly what they do there is not clear.

Potentially fatal mosquito-borne West Nile fever (WNF) can become much more widespread in Europe than previously thought, say scientists in a new report just out in the journal BMC Evolutionary Biology(1). The disease in temperate climates is carried by a population of Culex pipiens mosquitoes that only bites birds - the disease reservoir host - but Bruno Gomes and colleagues from the Centre for Malaria and Tropical diseases and Institute of Hygiene and Tropical Medicine in Portugal found high numbers of hybrids between this population and another one that bites on humans. These hybrids, by feeding on both humans and birds, can act as a bridge transmitting the disease to humans.
Abnormally high levels of P-cadherin – an adhesion molecule that enables cells to bind together – occur in about a third of all breast cancers and are associated with poor prognosis. Portuguese researchers , writing in the journal Oncogene1, found that the reason why these cancers are more aggressive is because excessive P-cadherin changes the cancer cells’ internal organization, making them mobile and invasive (invasiveness is the capacity to cross biological barriers such as membranes). Both these characteristics allow the formation of metastases - which is the spread of cancer cells from the original site of the tumour to other parts of the body - increasing the disease aggressiveness and explaining the poor prognoses associated with P-cadherin.
Cooperation is seen in every corner of life from microbes to humans, many times with no obvious advantages to those that provide it at high costs. Given the existence of “freeloading cheaters” ready to exploit the resources of those cooperating, why is it that cooperation persist? In an article now published in the journal Current Biology Nogueira and colleagues suggest that in bacteria this can result from highly mobile genes that “jump” from one cell to the next carrying the cooperative traits, effectively turning everyone into a cooperator. They also show that, at least in Escherichia coli (E. coli), this new population remains stable through “punisher” genes that impose a mafia-like strategy of “cooperation or death”, ensuring that the new cooperators do not revert to freeloading.