According to the latest US Alzheimer’s Association report, one in three seniors dies with Alzheimers 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, Alzheimers 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, a Research Data Alliance (EU-US-Australia) has been formed and held its inaugural 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 called AgedBrainSYSBIO – 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 the March 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.
Diseases include ALS and a form of dementia called IBMPFD
Single mutations in one gene rarely cause different diseases. New research, published in the journal Neuron, gives insight into how single mutations in the VCP gene cause a range of neurological conditions including the motor neuron disease Amyotrophic Lateral Sclerosis (ALS) and a form of dementia called Inclusion Body Myopathy, Paget’s Disease of the Bone and Frontotemporal Dementia (IBMPFD)
This study shows that these mutations disrupt energy production in cells shedding new light on the role of VCP in these multiple disorders.
Leading experts in neurodegeneration research met in Dublin on March 1st to discuss future research directions and opportunities to collaborate internationally.
In association with Irish representatives from the JPND Management Board, a scientific session was organised on March 1st, 2013, between prominent Irish researchers in the neurodegenerative disease field and JPND representatives.
The meeting was co-organised by JPND, the Health Research Board and Science Foundation Ireland to capitalise on the visit to Dublin of the JPND Chair, Philippe Amouyel, as part of the Irish presidency conference on Joint Programming.
An overview of the latest developments in basic and clinical research in Ireland and internationally was presented, with a selection of leading Irish researchers showcasing their most recent findings. Other JPND representatives at the session included:
Scientific Advisory Board – Prof. Philip Scheltens, VU Medical Center, The Netherlands
Steering Committee – Dr Rob Buckle, Medical Research Council, UK
Executive Board – Mr. Enda Connolly, Health Research Board
The programme for the meeting is available for download at the link below:
Genome-wide imaging study identifies a new gene called BCHE, found to be associated with Alzheimer’s plaques
The is the first genome-wide association study of plaque deposits using a specialized PET scan tracer that binds to amyloid – florbetapir. This imaging tracer allows physicians to see the level of plaque buildup in a patient’s brain, something that previously could be determined only with an autopsy. The researchers conducted PET scans of 555 participants in the Alzheimer’s Disease Neuroimaging Initiative, a long-term public-private research project that includes people at risk for Alzheimer’s disease and patients who have been diagnosed with the disease as well as participants with no symptoms. The analysis found that a variant in BCHE was significantly associated with the levels of plaque deposits.