Yearly Archives: 2014

The first follow-up conference to last December’s G8 Summit on Dementia took place recently in London to encourage leading nations to follow the commitments made in 2013.

The Global Dementia Legacy Event on Finance and Social Investment was held in London on 19 June 2014 and is the first of four global Legacy events that follow the G8 Dementia Summit.

The Medical Research Council (MRC) used the event to launch the world’s largest study group for research into dementias. In total two million people will take part in the £16 million project – called the UK Dementias Research Platform – led by the MRC in addition to support from partners pharmaceutical giants and smaller biotech companies.

Alzheimer’s Research UK (ARUK) also unveiled at the event a new “Defeat Dementia” campaign aiming to raise aiming to raise a minimum of £100 million over the next 5 years to defeat dementia and increase research innovation.

You can watch recordings of the full proceedings at the link below:

(see the question to Phillippe Amouyel, Chair of the JPND Management Board at 1:07:26 in the Session 2 video)

A new study suggests there could be a way to harness the brain’s capacity to self-repair and make new brain cells and perhaps preserve brain function in neurodegenerative diseases.

In Alzheimer’s, Parkinson’s, variant Creutzfeldt-Jakob and other brain-wasting prion diseases, cells in the brain gradually deteriorate, begin to function abnormally, and die. However, some parts of the brain have the capacity to self-repair and make new brain cells.

Writing in the journal Brain, study leader Dr. Diego Gomez-Nicola and colleagues from the Centre for Biological Sciences at the University of Southampton in the UK describe how previous studies have already revealed that even in neurodegenerative diseases there is evidence that the brain carries on attempting to repair itself.

One area of the brain that shows evidence of self-repair or neurogenesis is the dentate gyrus, which forms part of the hippocampus, which controls learning and memory.

Studying the brains of mice with a prion disease, the team found evidence of increased self-repair in the dentate gyrus that partially compensated for the loss of brain cells caused by the disease.

Their detailed investigation helped them identify how the new brain cell populations were generated over time, and how they integrated with existing brain circuits.

The team says they also found evidence to suggest increased self-repair in postmortem brain samples of patients who had variant Creutzfeldt-Jakob disease and Alzheimer’s disease when they died.

The authors conclude that the brain has some ability to orchestrate self-repair and suggest there is a time-limited window of opportunity for potential treatments to boost this mechanism and preserve brain function in patients with neurodegenerative diseases.

Source:  Medical News Today

A new report from Alzheimer’s Research UK, featuring analysis from Office of Health Economics (OHE), has modelled the impact of new treatments for dementia were they to be introduced in the UK from 2020.

The report entitled "Defeat Dementia: The evidence and a vision for action" reveals that a therapy delaying onset of dementia by five years would both reduce the number of cases by a third and alleviate economic costs by 36%, or over £21 billion, by 2050

Copy of Report:http://www.alzheimersresearchuk.org/siteFiles/resources/documents/reports/ARUK-OHE-report.pdf

Source:  ARUK

A nationwide study in Sweden of 19,743 dementia patients in the Swedish Dementia Registry found that cardiovascular medication is used extensively across dementia disorders and particularly in vascular and mixed dementia.

Several cardiovascular disorders have been suggested as risk factors for dementia, such as hypertension, hypercholesterolemia, atrial fibrillation and heart failure.

Correct management of these conditions can slow down cognitive decline, reduce the risk for dementia and maintain stability in patients with dementia.

The authors recommend that future research should investigate the tolerability and effectiveness of these drugs in the different dementia disorders.

Source:  Alzheimer’s Research and Therapy 

Writing in the June 12 PLOS Pathogens, researchers led by Olivier Andréoletti at the National Veterinary School of Toulouse, France, report a technique to detect tiny amounts of toxic prions in blood.

The researchers hope such a test will be used to determine the prevalence of latent vCJD in the European population, especially in the United Kingdom, where exposure to the disease was highest. Such a test could also prove useful for screening donor blood prior to transfusion, but a lack of political will prevents it from moving forward, according to Andréoletti and other researchers.

The study provides the first evidence that vCJD can be detected in asymptomatic primates, which most closely model the human forms of the disease.  The results suggest that asymptomatic human carriers may also be detected with the test. 

Source: AlzForum

The brain-training company Lumosity has opened its gaming database to researchers as part of what it calls the Human Cognition Project.

The database contains records of every mouse click from the 1.5 billion game sessions logged by the company’s 60 million users. Researchers from around the globe are sifting through it in search of patterns that may illuminate how aging, stress, sleep, and other lifestyle factors affect cognition. In particular, some scientists are panning the database for signatures of early decline that may flag people for prevention trials.

Some researchers believe that brain games in general—which adapt to each user’s cognitive ability—may one day serve as cognitive diagnostics to monitor progression or help enroll clinical trials.

More information available at the link below:

Source:  AlzForum

A team of researchers has demonstrated that immunotherapy with specifically targeted antibodies may block the development and spread of Parkinsons pathology in the brain.

Using powerful, newly developed cell culture and mouse models of sporadic Parkinson’s disease (PD), researchers intercepted the distorted and misfolded alpha-synuclein (alpha-syn) proteins that enter and propagate in neurons, which creating aggregates. This resulted in preventing the development of pathology and also reversed some of the effects of already-existing disease. The alpha-syn clumps, called Lewy bodies, eventually kill affected neurons, which leads to clinical PD.

The work appeared on June 16th in Cell Reports.

Source:  HealthCanal

Journal Article:http://www.cell.com/cell-reports/abstract/S2211-1247(14)00427-6

Researchers are not sure why spontaneous and unexplained disturbance in REM sleep should lead to a neurodegenerative disease like Parkinson’s

Presenting their research at the US Society of Nuclear Medicine and Molecular Imaging’s 2014 Annual Meeting, new longitudinal imaging data show a clear correlation between idiopathic REM behavior disorder and dysfunction of the dopamine transporter system involved in a wide range of vital brain functions, including memory and motor control.

A total of 21 consecutive patients with no known Parkinsonism or cognitive decline were enrolled in the long-term study between 2004 and 2006 and were followed after about 8 years. A baseline SPECT scan of dopamine transporter function was performed with the radiopharmaceutical I-123 FP-CIT as an imaging agent. A follow-up scan was performed to assess progression of neurodegenerative disease.

Results showed that after follow-up, patients’ SPECT scans revealed substantial decreases in radiotracer binding to the dopamine transport system in the nigrostriatal regions of the brain. A lack of tracer binding in these regions of the brain is closely linked to neuronal degeneration and the development of dementia and movement disorders.

Source:  The Freepress Journal

Researchers have found that depression leads to the increase of a naturally occurring protein in the brain (beta-amyloid) – a hallmark of Alzheimer’s disease.

Most of the aging population develops depression and this could be a major risk factor of developing Alzheimer’s faster than others.

"Our research results clearly indicate that mild cognitively impaired subjects with depressive symptoms suffer from elevated amyloid-levels when compared with non-depressed individuals," said the study’s principal scientist Axel Rominger, MD, from the department of nuclear medicine at the University of Munich in Germany. "The combination of elevated amyloid-levels and coexisting depressive symptoms constitute a patient population with a high risk for faster progression to Alzheimer’s disease."

The study included 371 patients with mild cognitive impairment who underwent PET imaging with radiotracer F-18 florbetapir and MRI. The subjects were chosen from Alzheimer’s Disease Neuroimaging Initiative database. The study also included data from 55 different research centers across the U.S. and Canada.

Source: Science World Report

A recent Lancet article assessed the impact of the French Alzheimer Plan (2008-2012). Government funding and coordination was provided by the Ministry of Health, the Alzheimer Foundation Plan and the French National Research Agency.

A bibliometric analysis, summarised in this article, raises interesting speculations on the relationship between public funding for dementia-related research and the resulting scientific productivity and innovation, as measured in terms of the ensuing quantity of high quality research publications.

Reference
Devos, P. Haeffner-Cavaillon, N. [and] Ledoux, S. [et al] (2014). Assessing the French Alzheimer plan. Lancet. May 24th 2014, Vol.383(9931), pp.1805.