Yearly Archives: 2013

A new laboratory study by scientists from Germany and the US shows that certain protein particles are indeed capable of multiplying and spreading from one cell to the next.

In diseases like Alzheimer’s and Parkinson’s endogenous proteins accumulate in the brain, eventually leading to the death of nerve cells. These deposits, which consist of abnormally formed proteins, are supposed to migrate between interconnected areas of the brain, thereby contributing to the development of the illness.

The investigation was conducted by researchers of the German Center for Neurodegenerative Diseases (DZNE) in Bonn and Munich who cooperated with scientists from the US and from other German institutions. The results are now published in the Proceedings of the National Academy of Sciences (PNAS). 

More information at the link below:

The flagship publication of the WHO Regional Office for Europe is issued every three years

The 2013 report covers the overall improvements to health in the European Region, and analyses the health inequalities within and across countries. A road-map is provided to Europe’s health policy goal, entitled “Health 2020”. The epidemiological evidence-base is presented for Health 2020.

Details in the 2013 report are outlined in four sections:

• Addressing health status in Europe
• European targets for health and well-being
• The case for measuring well-being
• An agenda to address measurement challenges

An executive summary of the report is available at the link below:

New study from the USA aimed at modeling the course of Parkinson’s disease (PD) which describes the economic consequences of slower rates of progression

Multiple studies describe progression, dementia rates, direct and indirect costs, and health utility by Hoehn and Yahr (H&Y) stage, but research has not incorporated these data into a model to evaluate possible economic consequences of slowing progression.

A Markov model was developed by the authors to show the net monetary benefits of slower rates of progression. Four scenarios assuming hypothetical slower rates of progression were compared to a base case scenario.

Base case results indicate average excess direct costs of $303,754, life-years of 12.8 years and quality-adjusted life-years of 6.96. A scenario where PD progressed 20% slower than the base case resulted in net monetary benefits of $60,657 ($75,891 including lost income) per patient. The net monetary benefit comes from a $37,927 decrease in direct medical costs, 0.45 increase in quality-adjusted life-years, and $15,235 decrease in lost income.

The scenario where PD progression was arrested resulted in net monetary benefits of $442,429 per patient. Reducing progression rates could produce significant economic benefit. This benefit is strongly dependent on the degree to which progression is slowed.

Study details how brain enzyme interacts with drug-like lead compound for Huntington’s Disease

Researchers at the Manchester Institute of Biotechnology have detailed how an enzyme in the brain interacts with an exciting drug-like lead compound for Huntington’s Disease to inhibit its activity. The research is published in the journal Nature.

Working with colleagues at the University of Leicester and the University of Lisbon in Portugal, the researchers identified the molecular structure of the enzyme kynurenine 3-monooxygense (KMO), which is found in the human brain. It took five years for the team to establish the crystal structure of KMO – the first time it’s ever been done.

The scientists then studied how the compound UPF 648 binds incredibly tightly to the enzyme to act as an inhibitor. Previous studies with animal models of neurodegenerative disease have showed that switching off the enzyme activity through drug binding should be effective in the treatment of brain disorders.

Professor Nigel Scrutton who led the study said: "UPF 648 works very well as an inhibitor of enzyme activity. However, in its current form it does not pass into the brain from the blood. The search is now on for related compounds that can both inhibit the enzyme and pass into the brain."

The findings from this research will now be used in the search for more effective treatments for Huntington’s Disease.

More information available at the links below:

According to the latest US Alzheimer’s Association report, one in three seniors dies with Alzheimer’s or another dementia in the United States.

The new report shows that while deaths from other major diseases, such as heart disease, HIV/AIDS and stroke, continue to experience significant declines, Alzheimer’s deaths continue to rise — increasing 68 percent from 2000-2010.

More information at the link below:

Promoting a shift to open science

It is generally accepted that outputs from publicly-funded research should be publicly available not only to researchers, but also to potential users in education, business, charitable and public sectors, and to the general public. 

The two major Open Access (OA) elements are OA for publications and OA for research data. These issues are under active consideration by a number of international initiatives. 

In this regard, aResearch Data Alliance  (EU-US-Australia) has been formed and held itsinaugural meeting on March 20th, 2013. The RDA alliance was formed initially by three research funding organisations:

• the Australian Commonwealth Government through the Australian National Data Service (www.ands.org.au)
• the European Commission through the iCordi project (www.icordi.eu)
• the United States of America through the RDA/US activity of the National Science Foundation (www.nsf.gov).

The goal of the alliance is to accelerate international data-driven innovation and discovery by facilitating research, data sharing and exchange, use and re-use, standards harmonisation for specific communities and across scientific disciplines.

More information is available at the link below:

A systems biology & comparative genomics approach for studying human brain ageing and/or most common age-related diseases

A new European group of academic laboratories and industrial scientists from SMEs will combine an integrative systems biology & comparative genomics approach for studying human brain ageing with a special emphasis on late-onset Alzheimer Disease. The objective will be to identify and validate new molecular targets and biomarkers.

The project is calledAgedBrainSYSBIO – systems biology of synapse proteins & ageing. AgedBrainSYSBIO is a European collaborative research project funded by the European Commission under the Health Work Programme of the 7th Framework Programme.

A new study supports the concept that prolonged and intensive environmental stimulation may have beneficial effects in delaying one of the key negative factors in Alzheimer’s disease.

It is well known that staying mentally active throughout life lowers the risk of developing Alzheimer’s disease, but how this works is unknown.

In theMarch 6 edition of Neuron, researchers reported that beta2-adrenergic signaling plays a key role. Wild-type mice that explored new toys every day had more synaptic plasticity and better resisted the toxic effects of ABeta oligomers compared to mice housed in the standard, boring cages. When researchers blocked the beta2-adrenergic pathway, the protection vanished. Conversely, feeding a beta2-adrenergic agonist to mice in the bland cages mimicked the benefit of an enriched environment.

Intriguingly, beta-adrenergic signaling has been shown to decline in AD brains.

Moreover, the scientists found that exposing the brain to novel activities in particular provided greater protection against Alzheimer’s disease than did just aerobic exercise. According to the researchers, this observation may be due to stimulation that occurred not only physically, but also mentally, when the mice moved quickly from one novel object to another.