Neuroendocrine-immunity in patients with Alzheimer's disease: toward translational epigenetics



Francesco Chiappelli1*, Paolo Prolo1, Kristine D. Cajulis1, Alberto Angeli2, Andrea Dovio2,Paola Perotti2, Marisa Pautasso3, Maria Luisa Sartori2, Laura Saba2, Stefano Mussino2, Thomas Fraccalini4, Fausto Fantó4, Ercolano Manfrini5, Cristina Mocellini6, Maria Gabriella Rosso6, Enzo Grasso6



1Division of Oral Biology & Medicine, UCLA School of Dentistry, Los Angeles, CA 90095-1668, West-Los Angeles, Veterans Administration Medical Center, Los Angeles, CA 90025; 2Internal Medicine, University of Turin, A.S.O. S. Luigi Gonzaga, Orbassano, Italy; 3Flow Cytometry Lab, University of Turin, A.S.O. S. Luigi Gonzaga, Orbassano, Italy; 4Geriatrics, University of Turin, A.S.O. S. Luigi Gonzaga, Orbassano, Italy; 5Department of Neurology, University of Ancona, Italy; 6Neurology, A.S.O. S. Croce e Carle, Cuneo, Italy


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Article Type

Current Trends


received April 14, 2007; accepted April 25, 2006; published online May 20, 2007



The emerging domain of epigenetics in molecular medicine finds challenging applications for a variety of patient populations.  Here, we present fundamental neuroendocrine-immune evidence obtained in patients with senile dementia of the Alzheimer’s type (sDAT), and discuss the implications of these data from the viewpoint of translational epigenetics of Alzheimer’s disease. We followed 18 subjects with mild sDAT treated with acetylcholinesterase inhibitors, and 10 control subjects matched for age in a repeated measure design every six months for 18 months. We monitored psychosocial profile (Mini-Mental State Examination, Functional Assessment Staging, Independence in Activities of Daily Living, Depression, Profile of Moods States) in parallel to immunophenotypic parameters of T cell subpopulations by flow cytometry. Based on change in the Mini-Mental State score at entry and at 18 months, patients with sDAT were assigned to a “fast progression” (Δ > 2 points) or to a “slow progression” group ( Δ  < 2 points). The change in circulating activated T cells (CD3+Dr+) with time in patients with sDAT was significantly inversely correlated with the change in time in natural killer (NK) cytotoxic activity to cortisol modulation in these patients, which was greater in patients with Fast Progression, compared to Slow Progression sDAT. These data indicate underlying neuroendocrine-immune processes during progression of sDAT. Our observations suggest that psycho-immune measures such as those we have monitored in this study provide relevant information about the evolving physiological modulation in patients with sDAT during progression of Alzheimer’s disease, and point to new or improved translational epigenetic treatment interventions.







Chiappelli et al., Bioinformation 2(1): 1-4 (2007)


Edited by

P. Kangueane






Biomedical Informatics



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