Lucio Tremolizzo


Dr. Lucio Tremolizzo, MD, PhD, is clinical neurologist at the ALS Center and at the Memory Clinic of the “San Gerardo” Hospital of Monza, Italy. At the same time, he coordinates the scientific activity of the Lab. of Neurobiology leaded by Prof. Carlo Ferrarese at the UNIMIB and teaches as Assistant Professor of Neurology. From 2001 to 2003 Dr. Tremolizzo has been post-doctoral research associate at the University of Illinois at Chicago. In the period 2005-2006 he has been honorary research assistant at the University College of London, obtaining the post graduate diploma in Clinical Neurology at the “Queen Square” Institute of Neurology.  For further details please visit his personal page on the website of the School of Medicine and Surgery.


  • Role of neuroinflammation in neurodegenerative disorders
  • Behavioral disturbances in dementia and amyotrophic lateral sclerosis
  • Relationship between amyotrophic lateral sclerosis and dementia
  • Epigenetics and neuropsychiatric disorders


Assessment of neuroinflammation during the initial phases of Alzheimer’s disease.

Aim: modulating chemotaxis and monocyte neuroinvasion.

Beta-amyloid, aggregating within the central nervous system (CNS), induces activation of microglia and migration of peripheral monocytes, in the attempt of limiting the deposition of this toxic peptide. These phenomena concur in determining a process of chronic brain neuroinflammation in patients affected by Alzheimer’s disease (AD).

This project studies the effect of anti-inflammatory drugs able to modulate the process of chemotaxis (and phagocytosis) carried out by monocytes/macrophages in prodromal/mild AD patients. The aim is reducing the propensity of monocytes to penetrate within the CNS. Analogously, we will measure serum markers correlated to this process, forming the “soluble arm” of the “inflammatory reflex”, able to further modulate monocyte phenotype and the process of chemotaxis/neuroinvasion. In particular, we will assess the ex vivo M1/M2 monocyte activation phenotype, pro-inflammatory, anti-inflammatory, and chemotactic cytokine expression (IL-6, IL-8, IL-10, IL-4, TNF-alpha, MCP-1, CXCL13), and the expression in mononucleated cells of TREM2, TSPO, nAChR, SOCS3. Moreover, we will prepare cell cultures for drug modulation of the above quoted parameters.


  1. Serum DBI and biomarkers of neuroinflammation in Alzheimer’s disease and delirium. Conti E, Andreoni S, Tomaselli D, Storti B, Brovelli F, Acampora R, Da Re F, Appollonio I, Ferrarese C, Tremolizzo L. Neurol Sci. 2021;42:1003-1007.
  2. Serum naturally occurring anti-TDP-43 auto-antibodies are increased in amyotrophic lateral sclerosis. Conti E, Sala G, Diamanti S, Casati M, Lunetta C, Gerardi F, Tarlarini C, Mosca L, Riva N, Falzone Y, Filippi M, Appollonio I, Ferrarese C, Tremolizzo L. Sci Rep. 2021;11:1978.
  3. Urinary neopterin, a new marker of the neuroinflammatory status in amyotrophic lateral sclerosis. Lunetta C, Lizio A, Gerardi F, Tarlarini C, Filippi M, Riva N, Tremolizzo L, Diamanti S, Dellanoce CC, Mosca L, Sansone VA, Campolo J. J Neurol. 2020 Dec;267(12):3609-3616.
  4. Irisin and BDNF serum levels and behavioral disturbances in Alzheimer’s disease. Conti E, Grana D, Stefanoni G, Corsini A, Botta M, Magni P, Aliprandi A, Lunetta C, Appollonio I, Ferrarese C, Tremolizzo L. Neurol Sci. 2019;40:1145-50.
  5. Serum irisin is upregulated in patients affected by amyotrophic lateral sclerosis and correlates with functional and metabolic status. Lunetta C, Lizio A, Tremolizzo L, Ruscica M, Macchi C, Riva N, Weydt P, Corradi E, Magni P, Sansone V. J Neurol. 2018;265:3001-8.