Marco Racchi
Marco Racchi
facebook: Marco Racchi
affiliation: Università di Pavia
research area(s): Neuroscience, Cell Biology
Course: Biomolecular Sciences and Biotechnology
University/Istitution: Istituto Universitario di Studi Superiori, Pavia
Associate Professor of Pharmacology, University of Pavia

• 1989 University of Milano (Italy), Pharmaceutical Chemistry and Technology Degree
• 1990-1992 Bowman Gray School of Medicine – Wake Forest University, Winston Salem NC USA, Post Doc
• 1994-1997 University of Milano (Italy), Research Doctorate in Biotechnology and Pharmacology
The research activity of Prof. Racchi is mainly oriented to the study of pathogenetic mechanisms underlying Alzheimer’s disease (AD) and other neurodegenerative disorders. One of the major focus of the research has been the study of the pharmacological regulation of the amyloid precursor protein (APP) metabolism, now extended to the study of the physiological functions of APP and its metabolic products. In addition, we recently identified the presence of a conformational variant of p53 in tissue samples of AD patients and studied both its possible use as diagnostic marker of the disease and also its potential involvement in AD pathogenesis. A second line of research is focused on the relationship between the activity of protein kinase C (PKC) signal transduction functions in aging and the hormonal regulation of gene expression relevant to PKC activity. These systems are key regulator of many common pathways that are altered during aging and in age related diseases such as AD.
Schettini G, Govoni S, Racchi M, Rodriguez G. Phosphorylation of APP-CTF-AICD domains and interaction with adaptor proteins: signal transduction and/or transcriptional role--relevance for Alzheimer pathology. J Neurochem. 2010 Dec;115(6):1299-308.
Lanni C, Nardinocchi L, Puca R, Stanga S, Uberti D, Memo M, Govoni S, D'Orazi G, Racchi M. Homeodomain interacting protein kinase 2: a target for Alzheimer's beta amyloid leading to misfolded p53 and inappropriate cell survival. PLoS One. 2010 Apr 14;5(4):e10171.
Lenzken SC, Stanga S, Lanni C, De Leonardis F, Govoni S, Racchi M. Recruitment of casein kinase 2 is involved in AbetaPP processing following cholinergic stimulation. J Alzheimers Dis. 2010;20(4):1133-41.
Lanni C, Racchi M, Stanga S, Mazzini G, Ranzenigo A, Polotti R, Memo M, Govoni S, Uberti D. Unfolded p53 in blood as a predictive signature signature of the transition from mild cognitive impairment to Alzheimer's disease. J Alzheimers Dis. 2010;20(1):97-104.
Del Vecchio I, Zuccotti A, Pisano F, Canneva F, Lenzken SC, Rousset F, Corsini E, Govoni S, Racchi M. Functional mapping of the promoter region of the GNB2L1 human gene coding for RACK1 scaffold protein. Gene. 2009 Feb 1;430(1-2):17-29.
Corsini E, Racchi M, Lucchi L, Donetti E, Bedoni M, Viviani B, Galli CL, Marinovich M. Skin immunosenescence: decreased receptor for activated C kinase-1 expression correlates with defective tumour necrosis factor-alpha production in epidermal cells. Br J Dermatol. 2009 Jan;160(1):16-25.
Project Title:
Physiopathology of AD and diagnostic biomarkers of the disease – Studies on p53 conformational mutant and its relevance to AD diagnosis and pathoge
We demonstrated that in Alzheimer’s disease, soluble beta amyloid (Aβ 1-40) has a modulatory effect on p53 by interfering with the homeodomain interacting protein kinase 2 (HIPK2), one of the major activators and controllers of p53. This suggest that cells where Aβ induce HIPK2 depletion and unfolded p53 may accumulate damage resulting in the survival of injured dysfunctional cells. We will investigate the mechanism through which Aβ leads to HIPK2 deregulation/degradation, to describe the mechanisms of HIPK2 activation/inhibition and its relationship to the correct control of cellular damage.

Project Title:
Aging and immunosenescence – Studies on the physiological and pharmacological regulation of RACK1 and PKC signalling in aging and immunosenescence
Aging is associated to a decline in immune functions that are in part related to a defective PKC dependent signal transduction machinery. Decrease in immune functions is a consequence of this signal transduction impairment. The purpose of this project is to investigate the role of glucocorticoids and dehydroepiandrosterone in the modulation of PKC and its anchoring protein RACK-1 functions.