Monthly Archives: október 2013

University of California Irvine’s trailblazing 90+ Study, aimed at learning more about the „oldest old, will continue for at least another five years, thanks to a $9.5 million renewal grant from the US National Institute on Aging.

The 90+ Study is among the largest studies of the oldest old in the world, with clinical, pathological and genetic research being conducted on more than 1,600 participants. Results obtained thus far have provided researchers across the globe with valuable information about aging."

The UC Irvine study is among the few to look at dementia in people over age 90. With the renewed round of funding over the next five years, 90+ researchers plan to employ PET and MRI scans to address these questions: Why do many of the oldest old have Alzheimer’s or vascular pathology in their brains but not show signs of dementia? Are they in the preclinical stages of disease? Will their cognitive abilities eventually decline?

The researchers also intend to monitor blood pressure and oxygen saturation over 24-hour spans to see if dips in blood pressure, particularly during the night, or periods of fluctuation are associated with cerebral microinfarctions or other diseases of the brain that can cause dementia.

Two 2-step calls are due to launch in early December 2013, with a likely first stage (pre-proposal submission) deadline of February 2014.

The EU Joint Programme – Neurodegenerative Disease Research (JPND) is implementing the priorities identified in itsResearch Strategy through a range of large-scale programmatic initiatives. 

During the first phase of implementation (2012-2014), JPND anticipates the launch of JPND Joint Transnational Calls each year to address high priority areas in neurodegenerative disease research*. 

JPND expects to launch two Joint Transnational Calls later this year aimed at supporting transnational collaborations in the field of neurodegenerative disease research.  The 2-step calls are anticipated to launch in early December 2013, with a likely first stage (pre-proposal submission) deadline of February 2014. 

Further detail will be provided here on the call launch date.  However, the indicative titles of each call are provided below:

“A call for European research projects for Cross-Disease Analysis of Pathways related to Neurodegenerative Diseases”

The aim of the call is to establish a limited number of ambitious, innovative, multi-national and multi-disciplinary collaborative research projects that;

  • combine experimental approaches from fundamental, pre-clinical and/or clinical with computational approaches
  • perform network analyses in different neurodegenerative and other chronic diseases to elucidate the underlying mechanisms common and differing in the investigated diseases
  • will add value to existing research by analysing diseases across traditional clinical boundaries, thereby gaining deeper understanding of the patho-physiological mechanisms of the diseases.

“A call for European research projects for Pilot Studies on Preventive Strategies related to Neurodegenerative Diseases”

The aim of the call is to establish pilot initiatives to develop preventive strategies. Proposals should entail multidisciplinary studies which may focus on new paradigms for multimodal preventive interventions including culture specific aspects, on harmonisation initiatives, or on proof-of-concept, and feasibility studies. Proposals may include research-based evaluation of interventions and validation of outcome measures.

Please Note:   

  • For both calls, JPND will pilot the use of a new online partnering tool. The tool will enable call applicants to showcase their research group’s expertise, search for appropriate partners, pitch call-related ideas and draft their pre- and full-proposals online. The tool will be made available through the JPND website, and will be announced in a JPND News alert in November 2013.Sign up here for JPND website alerts.
  • All information regarding future JPND Call topics is indicative and subject to change.

* The JPND diseases are:
Alzheimer’s disease (AD) and other dementias, Parkinson’s disease (PD) and PD-related disorders, Prion disease, Motor neurone diseases (MND), Huntington’s Disease (HD), Spinocerebellar ataxia (SCA), Spinal muscular atrophy (SMA)

A chemical substance has been identified which shows signs of being able to halt a range of neurodegenerative diseases in mice.

Researchers at the University of Leicester’s Medical Research Council Toxicology Unit, investigating prion disease in mice, have found a common feature across all types of brain cell death. Looking at the natural defence mechanisms of brain cells, they found that brain cells respond by shutting down protein production when attacked by a virus (in order to halt the virus’s spread).

A range of neurodegenerative diseases involve the formation of faulty or "misfolded" proteins, and these activate similar defence mechanisms. In Parkinson’s Disease it is alpha-synuclein which is the errant protein, in Alzheimer’s Disease it is amyloid and tau, and in the case of Huntingdon’s Disease it is another different protein.

The researchers believe the specific errant protein is irrelevant, because it is how cells deal with misfolded protein which is important. The presence of misfolded proteins causes brain cells to shut down protein production for a long period, eventually resulting in cell death.

The researchers believe they may be able to disrupt this process by the administration of a particular compound, thereby halting neurodegeneration; at least in mice with prion disease so far.

Research teams from Sheffield, UK and Milan, Italy looked at the factors which might explain the differences observed in speed and severity in the progression of motor neuron disease (MND).

Researchers used a scientific technique known as gene expression profiling to identify factors within motor neurones that control vulnerability or resistance to MND in order to shed light on the factors important for the speed of motor neurone injury in human patients.  The research, published in the scientific journal Brain, investigated two mouse models of MND caused by an alteration in the SOD1 gene, a known cause of MND in humans. One of the strains had a rapidly progressing disease course and the other a much slower change in the symptoms of MND.

The study, funded by the Motor Neurone Disease Association, revealed new evidence at the point of onset of the disease, before muscle weakness was observed, showing key differences in major molecular pathways and the way the protective systems of the body responded, between the profiles of the rapid progressing and slow progressing models. In the case of the model with rapidly progressing MND the motor neurones showed reduced functioning of the cellular systems for energy production, disposal of waste proteins and neuroprotection. Motor neurones from the model with more slowly progressing MND showed an increase in protective inflammation and immune responses and increased function of the mechanisms that protect motor neurones from damage.

Neurobiologists from the Friedrich Miescher Institute for Biomedical Research proved that excitability protects motor neurons from degeneration in amyotropic lateral sclerosis, a rare neurodegenerative disease.

By modulating excitability researchers could influence the rate of motor dysfunction and muscle denervation, and slow the progression rate of the disease.

This is important because it points to a possible way to delay the progression of this so far incurable disease.

Their results are published online in Neuron. 

Having depression may increase your risk of developing Parkinson’s disease by up to three times, according to a new study.

Depression is known to raise the risk of a host of diseases including cancer and stroke, but although it is known to be more common among Parkinson’s patients than the general population, it remains unclear whether it is a cause or a symptom.

Researchers from Taipei Veterans General Hospital in Taiwan examined the medical records of 4,634 people who suffered from clinically diagnosed depression, and 18,544 who did not, over a ten-year period.
They found that 66 people with depression, or 1.42 per cent, went on to be diagnosed with Parkinson’s during the next decade compared with 97 of those without depression, or 0.52 per cent.

After other factors such as age were taken into account, patients with depression were found to be 3.24 times more likely to be diagnosed with Parkinson’s than those without.

Even when researchers excluded the records of patients who were diagnosed with Parkinson’s shortly after their depression diagnosis, the link was still apparent suggesting that depression raises the risk of Parkinson’s over the long term.