Alan M. Palmer
Cerebroscience Ltd, United Kingdom
Alan M Palmer has formed or co-founded seven biotech start-up companies. He is presently a board director of Cerebroscience Ltd., MS Therapeutics Ltd, One Nucleus Ltd, Cerestim Ltd, Health e-games Ltd and the British Neuroscience Association. His career has focussed on CNS disorders and their treatment and, with over 100 peer-reviewed papers to his name, his scientifi c research has had a high impact in the areas of dementia and traumatic brain injury. He is visiting Professor at University College London and the University of Reading and Life Science Entrepreneur in Residence at the University of Bristol. He was voted London Biotechnology Network Entrepreneur of the Year in 2005.
The World’s population is increasingly ageing, as people are living longer and the babyboomer generation begins to reach age. This demographic shift will have many consequences, one of which is an increased burden of care for people with dementia, since its prevalence increases exponentially with age. More than 35 million people worldwide are now living with dementia and this number is expected to double by 2030 and more than triple by 2050. This, together with the high cost of long-term neurological care, means that dementia is an escalating international crisis. Alzheimer’s disease (AD) is the most common form of dementia. It impacts daily living through cognitive decline that usually starts with memory impairment and progresses, over a period of 8–10 years, to cause a more generalized cognitive dysfunction, behavioural dysregulation, and psychiatric symptoms. The emergence of symptoms reflects the largely predictable advance of degenerative changes in the brain. These include: (i) the formation of dystrophic neurites around a central core of amyloid (plaques); (ii) the formation of abnormal filaments (neurofibrillary tangles,NFTs) made up of a highly phosphorylated form of the microtubule- associated protein tau in the perikaryia of certain neurons (particularly pyramidal cells), along with neuropil threads in axons and nerve terminals; and (iii) the selective loss of neurons, principally pyramidal, cholinergic, noradrenergic and serotonergic neurons. Medicines that slow or stop the cascade of neurodegenerative change that characterises AD have the potential to reduce significantly the global burden of dementia. Thus, if a neuroprotective drug that delays disease onset by 5 years is introduced in 2015, it is predicted to reduce the number of those with clinical symptoms by over 40% in 2050. The discovery of such a medicine is critically dependent on understanding the biological basis of AD.