Monthly Archives: marzo 2018

Low muscle strength during the later teen years has been identified as a risk factor for much later onset of the neurological disease known as ALS, or amyotrophic lateral sclerosis.

A study published in the Journal of Neurology also links low blood counts at a young age to ALS.

The researchers studied Swedish military enlistment data for more than 1.8 million (1,819,817) men in the 1968-2005 period as well as data from the Swedish health care register and mortality register. The majority were 18 years old at the time of enlistment. The follow-up time was up to 46 years.

The group included 526 individuals who developed ALS, a disease that usually occurs after age 50 and involves a successive degradation of the nerves that control muscles. There is no cure, and in most cases patients die after two to five years.

The current study confirms the impression that ALS can be associated with a relatively low body mass index (BMI), even at a young age. The differences, however, were not dramatic. Those who developed ALS had an average BMI of 21.1, compared with 21.9 for the group as a whole.

What stood out instead was the finding that ALS could be associated with low blood counts at military enlistment – in other words, a low proportion of oxygen-carrying red blood cells in the blood. A link was also found between ALS and measured muscle strength in the hands, arms and legs at the time of enlistment.

Paper: “Risk factors in Swedish young men for amyotrophic lateral sclerosis in adulthood”
Reprinted from materials provided by the University of Gothenburg.

The UK Dementia Research Institute (UK DRI) is now recruiting an associate director to lead its care and technology programme. Candidates should have an exciting vision for how patient-focused research can lead to a significantly improved quality of life for people affected by dementia.

With a budget of £20 million, the new care and technology programme will be fully integrated into the wider institute, will benefit from its considerable resources and networks and, crucially, will embrace novel technologies and interdisciplinary approaches.

The deadline to apply is 17 April 2018.

To learn more and download the recruitment pack, please visit the UK DRI website.

With the aid of a PET camera, researchers have developed a new method for investigating the dopamine system in the brains of patients suffering from Parkinson’s disease. The method measures levels of a protein called dopamine transporter and could lead to improved diagnosis of Parkinson’s disease. The study was published in Movement Disorders.

Dopamine is a substance produced in the brain and is responsible for controlling our movements. In Parkinson’s disease, dopamine cells degenerate and their loss is responsible for the motor symptoms that characterise the disorder, such as shaking, slowness of movement and difficulty walking.

Using Positron Emission Tomography (PET), a group of researchers have measured the levels of the dopamine transporter protein DAT that regulates the levels of dopamine in the brain. DAT functions as a biomarker for dopamine cells and is present on the surface of the dopamine cells in the cell bodies, on the nerve fibres and on the nerve endings. By measuring where DAT is found, researchers have been able to map the presence of dopamine cells.

The study was based on 20 patients suffering from mild Parkinsonism and an equal number of healthy individuals. The results showed significantly lower amounts of DAT in nerve endings in the Parkinson’s patients than those not suffering from the disease.

Future studies will examine patients with more advanced Parkinson’s, in order to gain a greater understanding of the links between DAT and clinical variables such as motor symptoms and the various stages of the disease.

Paper: “Nigrostriatal dopamine transporter availability in early Parkinson’s disease”
Reprinted from materials provided by Karolinska Institutet.

The U.S. Alzheimer’s Association is now accepting letters of intent (LOI) for a new programme called GAAIN Exploration to Evaluate Novel Alzheimer’s Queries (GEENA-Q).

The Global Alzheimer’s Association Interactive Network (GAAIN) is a big data platform for cohort discovery and data exploration focused on Alzheimer’s disease and dementia. GAAIN provides tools that allow researchers to explore diverse clinical, health factor, genetic, and imaging datasets from data partners around the world. It currently has nearly 500,000 unique clinical records from nearly 30 clinical studies.

GEENA-Q will stimulate researchers to interrogate the federated GAAIN network for new discoveries in Alzheimer’s research. Applications are encouraged from research laboratories and teams around the world.

LOI must be received by 5:00 PM ET, on April 4, 2018.

To learn more, please visit the GAAIN website.

How should academia and industry collaborate to generate new diagnostic tools and therapies for neurodegenerative diseases?

At a workshop in Turin in October 2017, JPND brought together some 20 representatives from academia and the private sector to address this question and to lay the foundations for future exchanges and collaborations.

In a series of frank and lively discussion sessions, participants offered their views on the scientific areas and activities where potential exists for improved collaboration and alignment. Participants represented a broad range of sectors, including pharma, diagnostics, imaging, medical devices, and healthcare providers, and about half of the private-sector attendees came from small and medium-sized enterprises (SMEs).

During the discussions and in responses gathered by questionnaire, the three most important areas identified for potential collaboration – based on the scientific priorities of the JPND Research Strategy – were Developing therapies, preventive strategies and interventions, followed by Disease mechanisms and models and Origins of neurodegenerative diseases.

Participants identified science exchange programmes and infrastructure sharing as specific activities around which JPND and industry scientists could work together in the future. Other ideas identified from the brainstorming included organising a meeting for industry scientists focused on JPND research findings as well as inviting company scientists to join the review board for JPND calls. Direct participation in JPND calls was also encouraged, for example there could be a call to enable scientists who had developed promising products to interact with SMEs that specialized in product development.

JPND’s activities and new tools, including the Experimental Models for Parkinson’s Disease Database and the Global Cohort Portal, were also presented as part of the workshop.

The half-day meeting, which took place as part of the annual Meet in Italy for Life Sciences event, represented a first step toward improved engagement with industry and SMEs, and the outputs will be further analysed to improve JPND’s ongoing and future strategy for engagement with industry.

A team of researchers has found that gradually depleting an enzyme called BACE1 reverses the formation of amyloid plaques in the brains of mice with Alzheimer’s disease, thereby improving the animals’ cognitive function. The study was published in the Journal of Experimental Medicine.

An early event in Alzheimer’s is the abnormal buildup of beta-amyloid peptide, which can form large amyloid plaques in the brain and disrupt the function of neuronal synapses. BACE1 helps produce beta-amyloid peptide by cleaving amyloid precursor protein (APP).

Researchers have hypothesized that inhibiting BACE1 could keep the plaques from appearing. However, BACE1 controls many important processes by cleaving proteins other than APP, and mice completely lacking BACE1 have been shown to suffer severe neurodevelopmental defects.  For this study, the researchers  generated mice that gradually lose this enzyme as they grow older. These mice were shown to develop normally and appeared to remain perfectly healthy over time.

The researchers then bred these rodents with Alzheimer’s mice. The resulting offspring also formed plaques at this age, even though their BACE1 levels were approximately 50% lower than normal. Remarkably, however, the plaques began to disappear as the mice continued to age and lose BACE1 activity, until, at 10 months old, the mice had no plaques in their brains at all.

Decreasing BACE1 activity also resulted in lower beta-amyloid peptide levels and reversed other hallmarks of Alzheimer’s disease, such as the activation of microglial cells and the formation of abnormal neuronal processes.

Loss of BACE1 also improved the learning and memory of mice with Alzheimer’s disease. However, when the researchers made electrophysiological recordings of neurons from these animals, they found that depletion of BACE1 only partially restored synaptic function, suggesting that BACE1 may be required for optimal synaptic activity and cognition.

Article: “BACE1 deletion in the adult mouse reverses preformed amyloid deposition and improves cognitive functions”
Reprinted from materials provided by Rockefeller University.

Scientists have developed a novel approach for deep brain stimulation. The new method, published in Science, utilises upconversion nanoparticles to allow delivery of visible light deep into the brain to stimulate neural activities in a less-invasive manner. This innovation marks a significant breakthrough in optogenetics, empowering researchers to uncover valuable insights about the brain.

Optogenetics is a widely adopted research technique in the field of neuroscience that makes use of visible light to activate or inhibit neurons in the brain, enabling researchers to examine the brain’s functions in a minimally invasive manner. The inability of visible light to penetrate into deep brain structures, however, remains a major experimental challenge for this technique, and current deep brain stimulation still requires the insertion of an optical fibre directly into the brain.

To make deep brain stimulation less invasive, the researchers began exploring with near-infrared light, known to possess significantly higher tissue penetration capability and also relatively safe for biological samples. Using a two-step process, upconversion nanoparticles are first introduced into the brain by transcranial injection. Upon reaching deep brain, the implanted upconversion nanoparticles, a unique group of luminescent nanomaterials capable of converting near-infrared light into visible light, then generates visible light which acts to stimulate the neurons. The strategy has shown to be effective in triggering memory recall and dopamine release in the team’s experiments.

This novel approach offers a simpler, less-invasive alternative to fibre-optic implantation for deep brain stimulation, the researchers say, and holds immense potential in facilitating advancement in neuroscience.

Paper: “Near-infrared deep brain stimulation via upconversion nanoparticle–mediated optogenetics”

Reprinted from materials provided by the National University of Singapore.