Symptoms of Alzheimer's disease include loss of memory and cognitive impairment in sufferers. The disease is characterised by the deposition of self-assembled proteins in the form of Amyloid plaques and Neurofibrillary tangles comprised of Abeta and tau proteins respectively.
Dementia Research Group
Alzheimer’s disease (AD) is the commonest cause of dementia. Current treatments for AD provide only short term symptomatic benefit and efforts to date to identify therapies with the ability to slow down or prevent progression of disease have been unsuccessful.
Identification of effective therapies remains of paramount importance and there is an urgent need to address the underlying reasons behind the successive failures. There are three main reasons for these failures:
1) there remain significant knowledge gaps in understanding of AD pathophysiology, and these gaps hinder progress in drug discovery. Specifically, there remains significant uncertainty about the mechanisms by which the amyloid-beta peptide, an acknowledged central component of AD pathology, causes neuronal toxicity which leads ultimately to neuronal dysfunction and death.
2) it is widely accepted that AD patients used in previous trials have been too advanced in their disease and that future disease-modifying therapies are likely to exert greater beneficial effect if applied earlier in the disease. To address this, it is essential that early markers for AD are first identified.
3) the choice of optimal outcome measures by which to measure treatment effect in AD trials has yet to be determined.
The Dementia Research Group is a group of Researchers based at the University of Sussex and Brighton and Sussex Medical School who aim to address these knowledge gaps by focusing on greater understanding of the underlying mechanisms of disease in AD. This network encompasses neuroscientists, structural biologists, psychologists, clinicians and members of the translational drug discovery group. By exploring mechanisms of disease at the level of protein biochemistry and neuronal function, and translating this through animal models of disease to evaluation of disease effect on brain function in both healthy individuals and patients with early AD, this collective research effort will facilitate efforts to identify biomarkers of early AD as well as drug discovery programmes aimed at identifying novel therapeutic targets and their application to at-risk individuals in order to prevent or delay onset of AD.