Monthly Archives: April 2015

Although past research has associated obesity with increased risk of dementia, a new study – deemed the largest ever to assess the link between body mass index and dementia risk – suggests obesity could actually be a protective factor against the condition, while people who are underweight may be at increased risk.

A large retrospective cohort study, published in The Lancet Diabetes and Endocrinology, has revealed a surprising association between being underweight in mid-life and late-life, and increased risk of dementia.

The study assessed the medical records of almost 2 million people in the UK in order to gain a better understanding of how obesity affects dementia risk. The researchers found that, compared with adults who had a healthy BMI (between 20-25 kg/m2), those who were underweight – defined in this study as a BMI less than 20 kg/m2 – during middle age were 34% more likely to be diagnosed with dementia. This increased risk remained for 15 years after adults’ underweight status was recorded.

The team notes that participants with a BMI of less than 18.5 kg/m2 are usually classed as underweight, but the threshold was raised in this study to allow comparisons with past studies, which have defined a BMI of less than 20 kg/m2 as underweight.

The researchers also found that middle-aged adults’ risk of dementia steadily reduced as their BMI increased. Compared with adults who had a healthy BMI, those who were severely obese (BMI greater than 40 kg/m2) were 29% less likely to develop dementia. The team says their results remained even after accounting for factors associated with increased dementia risk, including smoking and alcohol consumption. In addition, the results were not affected by adults’ age at dementia diagnosis or the decade in which they were born, according to the researchers.

Source: Medical News Today

New research highlights how nerves – whether harmed by disease or traumatic injury – start to die, a discovery that unveils novel targets for developing drugs to slow or halt peripheral neuropathies and devastating neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis (ALS).

Peripheral neuropathy damages nerves in the body’s extremities and can cause unrelenting pain, stinging, burning, itching and sensitivity to touch. The condition is commonly associated with diabetes or develops as a side effect of chemotherapy.

Nerve cells talk to each other by transmitting signals along communication cables called axons. Such signals underlie vital activities, such as thinking and memory, movement and language. As part of the study, the researchers showed they could prevent axons from dying, a finding that suggests therapies could be developed to counteract the withering away of nerve axons.

The research, by scientists at Washington University School of Medicine in St. Louis, is reported online April 23 in the journal Science.

“We have uncovered new details that let us piece together a major pathway involved in axon degeneration,” said senior author Jeffrey Milbrandt, MD, PhD, the James S. McDonnell Professor and head of the Department of Genetics. “This is an important step forward and helps to identify new therapeutic targets. That we were able to block axon degeneration in the lab also gives us hope that drugs could be developed to treat patients suffering from a variety of neurological conditions.”

A common thread among many neurological disorders and traumatic nerve injuries is the degeneration of axons, which interrupts nerve signaling and prevents nerves from communicating with one another. Axon degeneration is thought to be an initiating event in many of these disorders. In fact, an unhealthy axon is known to trigger its own death, and researchers are keenly interested in understanding how this happens.

Working in cell cultures, fruit flies and mice, Milbrandt and co-author Aaron DiAntonio, MD, PhD, the Alan A. and Edith L. Wolff Professor of Developmental Biology, and their colleagues showed that a protein already known to be involved in axon degeneration, acts like a switch to trigger axon degeneration after an injury.

Moreover, they found that this protein, once unleashed, causes a rapid decline in the energy supply within axons. Within minutes after the protein – called SARM1 – is activated in neurons, a massive loss of nicotinamide adenine dinucleotide (NAD), a chemical central to a cell’s energy production, occurs within the axon.


The Joint Programming initiative (JPI) “More Years, Better Lives“ aims at coordinating national and European research activities in the field of demographic change.

The first call of Joint Programming Initiative (JPI) “More Years, Better Lives” was officially launched on 1 April 2015. The call covers the topic ”Extended Working Life and its Interaction with Health, Wellbeing and Beyond”.

7 million Euros will be allocated to the call by ten participating countries (Belgium, Denmark, Germany, Finland, Spain, Sweden, the Netherlands, Canada, the United Kingdom and Austria). The submission tool is open as of 18. April 2015. The Call deadline is 2 June 2015.

More information on the call is available at the link below:

In their latest brain imaging study on women at risk for Alzheimer’s disease, York University researchers have found deterioration in the pathways that serve to communicate signals between different brain regions needed for performing everyday activities such as driving a car or using a computer.

“We observed a relationship between the levels of deterioration in the brain wiring and their performance on our task that required simultaneous thinking and moving; what we see here is a result of communication failure,” explains Professor Lauren Sergio in the School of Kinesiology & Health Science.

In an interview, Sergio in whose lab the study was conducted, says the findings also suggest that their computerized, easily-administered task that the study participants performed, can be used to test those at risk for Alzheimer’s disease to flag early warning signs. “The test is a clinically feasible substitute to the more involved braining imaging tasks that people don’t, or can’t, have done routinely.”

The study, Diffusion Tensor Imaging Correlates of Cognitive-Motor Decline in Normal Aging and Increased Alzheimer’s Disease Risk, recently published in the Journal of Alzheimer’s Disease, was conducted on 30 female participants of whom 10 were in their mid-20s. The rest were in their 50s or older, with half of them at high risk for Alzheimer’s disease.

“We decided to focus this study on women, as there is higher prevalence in this group, and also women who carry the ApoE4 gene are more vulnerable to the degradation of white matter,” notes PhD candidate Kara Hawkins who led the study, adding that the genetic risk factor for Alzheimer’s disease was one of the traits tested for in the current study.

“We scanned the brains of the participants, aiming to see if the impaired cognitive-motor performance in the high risk group was related to brain alterations over and above standard aging changes,” Hawkins adds.

According to the researchers, the big question ahead is ‘what can be done to prevent a decline in function of a person’s brain showing signs of communication problems.’ And the answer they are exploring is in finding ways to use these thinking and moving tasks in a proactive way, as part of a game-like cognitive-motor integration training method


Translational research for neurodegenerative disease depends intimately upon animal models. Unfortunately, promising therapies developed using mouse models mostly fail in clinical trials, highlighting uncertainty about how well mouse models mimic human neurodegenerative disease at the molecular level.

This study compared the transcriptional signature of neurodegeneration in mouse models of Alzheimer׳s disease (AD), Parkinson׳s disease (PD), Huntington׳s disease (HD) and amyotrophic lateral sclerosis (ALS) to human disease.

In contrast to aging, which demonstrated a conserved transcriptome between humans and mice, only 3 of 19 animal models showed significant enrichment for gene sets comprising the most dysregulated up- and down-regulated human genes. Spearman׳s correlation analysis revealed even healthy human aging to be more closely related to human neurodegeneration than any mouse model of AD, PD, ALS or HD.

Remarkably, mouse models frequently upregulated stress response genes that were consistently downregulated in human diseases. Among potential alternate models of neurodegeneration, mouse prion disease outperformed all other disease-specific models.

Even among the best available animal models, conserved differences between mouse and human transcriptomes were found across multiple animal model versus human disease comparisons, surprisingly, even including aging. Relative to mouse models, mouse disease signatures demonstrated consistent trends toward preserved mitochondrial function protein catabolism, DNA repair responses, and chromatin maintenance. These findings suggest a more complex and multifactorial pathophysiology in human neurodegeneration than is captured through standard animal models, and suggest that even among conserved physiological processes such as aging, mice are less prone to exhibit neurodegeneration-like changes.

This work may help explain the poor track record of mouse-based translational therapies for neurodegeneration and provides a path forward to critically evaluate and improve animal models of human disease.

The Joint Programming Initiative “A Healthy Diet for A Healthy Life” has launched a joint transnational call for research proposals in the area of Nutrition and Cognitive Function.

The joint action “Nutrition and Cognitive Function” (NutriCog) aims at promoting research activities that address the interrelation of diet and cognitive function. This knowledge will lay the basis for dietary preventive strategies and recommendations to guide individuals and populations towards health promoting dietary habits.

The objective of the NutriCog Call is to support ambitious, innovative and transnational collaborative research projects that will address important questions relating to the interplay between nutrition and cognitive function. Both the influence of dietary patterns (and/or dietary constituents, where appropriate) on cognitive functions and vice versa the effects of Central Nervous System nutrient signaling and cognitive processes on food intake, dietary patterns and eating behaviour are relevant for this call.

Proposals have to follow a multidisciplinary approach and should cover multiple areas, such as mechanistic/experimental research, translational research, epidemiological research and pilot/proof of principle studies for interventions.

Source: JPI-HDHL

Five months into his five-year term as research commissioner, Carlos Moedas spoke to Nature Magazine about his hopes and ambitions for the scientific programmes run by the European Union (EU), particularly the huge seven-year €80-billion (US$86-billion) Horizon 2020 (H2020) research programme, which runs until 2020.

Moedas wants scientists to change their mentality for H2020, breaking free of individual silos and including more social science. But he is already facing complaints that money is being stripped from the programme to finance other European initiatives, such as the proposed €16-billion European Fund for Strategic Investment (EFSI), a Europe-wide bid to stimulate the region’s economy.

An edited version of the interview is available through the link below:

Source: Nature Magazine