Short report
Alzheimer's disease: new diagnostic and therapeutic tools
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* Corresponding author: Marco Racchi marco.racchi@unipv.it
1 Department of Experimental and Applied Pharmacology, University of Pavia, Italy
2 Department of Biomedical Sciences and Biotechnologies, University of Brescia, Italy
3 Immunosenescence Unit, Department of Pathobiology and Biomedical Methodologies, University of Palermo, Italy
4 Neurological Science Institute, National Research Council, Catania, Italy
5 Department of Health Sciences, University of Molise, Campobasso, Italy
Immunity & Ageing 2008, 5:7 doi:10.1186/1742-4933-5-7
Published: 13 August 2008Abstract
On March 19, 2008 a Symposium on Pathophysiology of Ageing and Age-Related diseases was held in Palermo, Italy. Here, the lectures of M. Racchi on History and future perspectives of Alzheimer Biomarkers and of G. Scapagnini on Cellular Stress Response and Brain Ageing are summarized. Alzheimer's disease (AD) is a heterogeneous and progressive neurodegenerative disease, which in Western society mainly accounts for clinica dementia. AD prevention is an important goal of ongoing research. Two objectives must be accomplished to make prevention feasible: i) individuals at high risk of AD need to be identified before the earliest symptoms become evident, by which time extensive neurodegeneration has already occurred and intervention to prevent the disease is likely to be less successful and ii) safe and effective interventions need to be developed that lead to a decrease in expression of this pathology. On the whole, data here reviewed strongly suggest that the measurement of conformationally altered p53 in blood cells has a high ability to discriminate AD cases from normal ageing, Parkinson's disease and other dementias. On the other hand, available data on the involvement of curcumin in restoring cellular homeostasis and rebalancing redox equilibrium, suggest that curcumin might be a useful adjunct in the treatment of neurodegenerative illnesses characterized by inflammation, such as AD.