Brains for Dementia Research, an initiative by Alzheimer’s Society and Alzheimer’s Research UK in association with the Medical Research Council seeks to address the shortage of high quality brains from people with and without dementia, available to researchers. This is a good opportunity for BGS colleagues to contribute to an important research function in an area of medicine that is part of their day to day work.
In 2008, Brains for Dementia (BDR) started recruiting people with dementia (any age) and those without dementia (over 65 years) to take part in serial standard psychometric assessments leading to brain and spinal cord donation at death. There are 6 centres based around leading dementia brain banks in London, Manchester, Newcastle, Bristol, Oxford and Cardiff (brain donations are stored in London) and increasing involvement of Clinical Research Networks has greatly extended geographical coverage.Funding has been extended to 2018, following successful peer review. The number of participants signed up for the project stands at just over 2,000, with approximately 65 per cent of those currently without dementia. To date we have received 215 brain with or without spinal cords, including 50 brains suitable for use as controls. This is exceptionally significant, as there is a particular shortage of brains from people dying without dementia, which has hugely hampered research efforts.
Many existing BDR participants were recruited from other studies, or heard about the project through the national press, or newsletters sent out by our funding charities and continued funding means that we can expand the cohort to a steady state (excluding donations) of between 3,000 and 3,500 over the next 2-3 years. From a participant’s perspective BDR provides an opportunity for those affected by dementia and their families to be involved in research to find new treatments and eventually a cure for dementia.
There has been a fantastic response from the research community, who can see the unique benefit of post-mortem brain material from people where their journey through dementia or their continued mental health is documented in a standard manner providing cognitive and behavioural data linked with genetic factors and chemical and pathological changes. The brain tissue is managed through an online database which researchers can search and apply to for samples. Tissue samples have been widely requested in UK and abroad, to date 47 requests have been made for brain samples BDR tissue has been acknowledged in 25 high quality publications, contributing to the advanced knowledge of the causes of dementia and the development of new treatments. Below are two recent examples.
“Long term incidence of dementia, predictors of mortality and pathological diagnosis in older stroke survivors”, L Allan et al., Brain, 2011:
Scientists at Newcastle University gained a greater understanding of the risk factors for dementia in stroke survivors. They followed 355 participants who had strokes, comparing their memory and thinking skills during life with changes in their brain after death. The researchers found a higher risk of dementia in stroke-survivors that also had three or more other vascular risk factors. The findings suggest that treatment and monitoring of these risk factors may help prevent dementia in people who have had a stroke.
“The role of a receptor protein GPR3 and modulatory molecules call beta arrestins in the generation of Aβ”, Bart De Strooper, et al, VIB centre for the Biology of Disease, Leuven, Belgium
This study provides an example of how research on brain tissue can help develop new treatment strategies. Deposition of Beta amyloid in the brain in AD is still considered by many to be one of the major factors contributing to the damage to neurones. Researchers have uncovered one of the processes that controls beta amyloid production, the G Protein linked receptors (GPR) system which is located in, and contributes to signalling across, the cell membrane. They found that one of the receptors in this family, GPR3, is elevated in AD. As this receptor can be controlled by a protein called β-arrestin, it may be possible to develop a beta amyloid lowering strategy based on this mechanism.