Monthly Archives: Março 2016

Accumulation of amyloid beta in the brain impairs memory and cognitive ability in people with Alzheimer’s. New findings published in Nature Communications show that the cause of amyloid beta pathology might be more versatile than previously known. Researchers believe that these new findings may be of significance to the development of new medications.

The accumulation of the protein amyloid beta in the brain is a sign of Alzheimer’s disease. Sufficiently large quantities cause plaque, which blocks the function of the nerve cells and thereby impair the patient’s memory and cognitive ability.

A small proportion of Alzheimer’s patients have a hereditary risk gene, which causes overproduction of amyloid beta in the brain. In all other cases, the cause of the disease has so far been explained by the body’s lack of ability to break down and remove amyloid beta. However, these new findings provide a more nuanced picture:

“In our study, we show that accumulation of amyloid in the brain is associated with high levels of specific amyloid peptides in the cerebrospinal fluid. This means that overproduction of amyloid beta may contribute to development of Alzheimer’s disease in some people, even if they do not carry the hereditary risk gene for Alzheimer’s. The fact that the disease in these individuals can be attributed to both the overproduction of and problems in breaking down amyloid beta may be of significance to the future development of drugs and treatments”, explained Niklas Mattsson, a researcher at Lund University and specialist physician at Skåne University Hospital.

The study noted increased levels of amyloid beta in a large group of patients with no hereditary risk gene. More than 330 people from Sweden participated in the study, some of whom suffered from mild cognitive disorders (which may be an early sign of Alzheimer’s), while others were part of a control group of healthy individuals.

Source: Lund University

An innovative tool allows researchers to observe protein aggregation throughout the life of a worm. The development of these aggregates, which play a role in the onset of a number of neurodegenerative diseases, can now be monitored automatically and in real time. This breakthrough was made possible by isolating worms in tiny microfluidic chambers.

Biologists and microfluidics specialists have joined forces and developed a highly innovative research tool: a 2cm by 2cm ‘chip’ with 32 independent compartments, each of which is designed to hold a nematode – a widely used worm in the research world. The device is described in the journal Molecular Neurodegeneration.

Each of these ‘cells’ is fed by microfluidic channels. These allow variable concentrations of nutrients or therapeutic molecules to be injected with precision. The ambient temperature can also be adjusted. Each worm is observed through a microscope throughout its life. However, for more detailed investigations and very high resolution images, the worms need to be immobilized.

This method is fully reversible and does not affect the nematode’s development. Using it, researchers can observe the formation of protein aggregates linked to several neurodegenerative diseases like Alzheimer’s, Parkinson’s and Huntington’s. The same worm can be photographed several times, as the clusters develop.

Nematodes are very useful models for studying a number of human diseases. In many cases, they obviate the need to experiment on rodents. But until now, handling nematodes was a delicate affair. By simplifying the process, this new technology should accelerate research on numerous afflictions and how they are treated.

Source: Emmanuel Barraud, École polytechnique fédérale de Lausanne

A study published in Scientific Reports demonstrates, for the first time and using computational tools, that polyunsaturated lipids can alter the binding rate of two types of receivers involved in certain nervous system diseases.

Using latest-generation molecular simulations, which are like “computational microscopes,” the researchers have demonstrated that a decrease in polyunsaturated lipids in neuronal membranes, as seen in Parkinson’s and Alzheimer’s sufferers, directly affects the binding rate of dopamine and adenosine receptors. These are part of the family of receptors connected to the G protein (GPCR), located in the cell membrane and responsible for transmitting signals to within the cell. Various studies have demonstrated that lipid profiles in the brains of people with diseases like Alzheimer’s and Parkinson’s are very different from those of healthy people. These studies showed that the levels of a polyunsaturated fatty acid in neuronal membranes are considerably lower in the brains of sufferers. The researchers believe that this difference in the lipid composition of membranes could alter the way in which certain proteins interact with each other, as in the case of the GPCR receivers.

These results could enable, in the future, new therapeutic pathways to be initiated for regulating the binding of these receivers, either through the lipid composition of the membrane or by designing new lipids that have a modulating effect on this binding rate. It could also facilitate the study of other similar scenarios where specific membrane lipids are able to modulate the behaviour of other important receivers, at a clinical level.

Source: Hospital del Mar Medical Research Institute

A new study in the journal Nature Communications shows that cells normally associated with protecting the brain from infection and injury also play an important role in rewiring the connections between nerve cells.  While this discovery sheds new light on the mechanics of neuroplasticity, it could also help explain diseases like autism spectrum disorders, schizophrenia, and dementia, which may arise when this process breaks down and connections between brain cells are not formed or removed correctly.

While the constant reorganization of neural networks – called neuroplasticity – has been well understood for some time, the basic mechanisms by which connections between brain cells are made and broken have eluded scientists.

Performing experiments in mice, the researchers employed a well-established model of measuring neuroplasticity by observing how cells reorganize their connections when visual information received by the brain is reduced from two eyes to one.

The researchers found that in the mice’s brains microglia responded rapidly to changes in neuronal activity as the brain adapted to processing information from only one eye.  They observed that the microglia targeted the synaptic cleft – the business end of the connection that transmits signals between neurons.  The microglia “pulled up” the appropriate connections, physically disconnecting one neuron from another, while leaving other important connections intact.

The researchers also pinpointed one of the key molecular mechanisms in this process and observed that when a single receptor – called P2Y12 – was turned off the microglia ceased removing the connections between neurons.

These findings may provide new insight into disorders that are the characterized by sensory or cognitive dysfunction, such as autism spectrum disorders, schizophrenia, and dementia.  It is possible that when the microglia’s synapse pruning function is interrupted or when the cells mistakenly remove the wrong connections – perhaps due to genetic factors or because the cells are too occupied elsewhere fighting an infection or injury – the result is impaired signaling between brain cells.

Source: University of Rochester Medical Center (URMC)

The Active and Assisted Living Programme (AAL), which aims to improve the conditions of life for older adults through the use information and communication technology (ICT), has opened its 2016 call, Living well with dementia.

The objective of the call is to advance the contribution of ICT to integrated solutions that enable the well being of people living with dementia and their communities, including their family, caregivers, neighbourhood, service providers and care system. The call aims to support innovative, transnational and multi-disciplinary collaborative projects with a clear route to market and added value for the different types of end users. A key priority underlying this challenge will be to bring together technologies and services to create ICT-based solutions addressing the specific aspirations and challenges of people living with dementia and their communities.

The submission deadline is 26 May 2016, 5PM CET. To learn more about the call or to register to watch the live webcast on 8 March, please visit the AAL website.