Richens Joanna L, Morgan Kevin, O'Shea Paul
Cell Biophysics Group, School of Life Sciences, Faculty of Medicine & Health Sciences, University Park, University of Nottingham, Nottingham, UK.
Humans Genetics Research Group, School of Life Sciences, Faculty of Medicine & Health Sciences, University of Nottingham, Queen's Medical Centre, Nottingham, UK.
Neurobiol Aging. 2014 Sep;35(9):2029-38. doi: 10.1016/j.neurobiolaging.2014.02.024. Epub 2014 Mar 2.
Alzheimer's disease (AD) poses an increasingly profound problem to society, yet progress toward a genuine understanding of the disease remains worryingly slow. Perhaps, the most outstanding problem with the biology of AD is the question of its mechanistic origins, that is, it remains unclear wherein the molecular failures occur that underlie the disease. We demonstrate how molecular biomarkers could help define the nature of AD in terms of the early biochemical events that correlate with disease progression. We use a novel panel of biomolecules that appears in cerebrospinal fluid of AD patients. As changes in the relative abundance of these molecular markers are associated with progression to AD from mild cognitive impairment, we make the assumption that by tracking their origins we can identify the biochemical conditions that predispose their presence and consequently cause the onset of AD. We couple these protein markers with an analysis of a series of genetic factors and together this hypothesis essentially allows us to redefine AD in terms of the molecular pathways that underlie the disease.
