Gender	Female
E-mail	cristina.alberini@mssm.edu
Education and Training	Laurea, University of Pavia
	Ph.D., University of Genoa
	Post-Doctoral Fellow, Dana Farber Cancer Institute
	Post-Doctoral Fellow, Columbia University

After training in biology and immunology, I have now focused my interest on how the brain changes in response to external and internal stimuli.  In particular, I am intrigued by how memories are formed, stored and elaborated.  Memory is a fundamental biological function and a critical component of our identity. As such, it involves our brain, mind and psyche. I am interested in exploring the biological mechanisms of memory and their integration into complex behavioral manifestations. I am also interested in applying this knowledge in order to understand how memory becomes an integral part of pathologies such as addiction and trauma.

Visit Dr. Cristina Alberini's Neurobiology of Learning and Memory for more information.

Education and Training	Laurea, University of Pavia
	Ph.D., University of Genoa
	Post-Doctoral Fellow, Dana Farber Cancer Institute
	Post-Doctoral Fellow, Columbia University

Specific Clinical/Research Interest: Molecular mechanisms of long-term memory

Current Students: MD/PhD: Dillon Chen; PhD: Dhananjay Bambah-mukku, Justin Riceberg

Postdoctoral Fellows: Elizaveta Muravieva, Carmen Inda, Akinobu Suzuki

Research Personnel: Gabriella Pollonini, Suzanna Katz

Summary of Research Studies:
A fascinating aspect of learning and memory is its biological basis. In order to occur, long-term memory requires an initial and relatively brief temporal phase during which gene expression is essential (consolidation phase). This is a universal feature of long-term memory processes, which is found in several different forms of memory and conserved throughout evolution. We are interested in the identification and functional characterization of the gene cascade activated during memory consolidation. In addition, our studies aim at determining where in the brain and when following learning this gene cascade is activated.

Our current approach is focused on differential gene expression screenings in specific brain areas of control, naive animals vs. animals that underwent learning. The identification of memory gene candidates is followed by molecular and functional studies aimed at defining the role of each identified component. We are also interested in understanding the molecular mechanisms that accompany memory reorganization after recall. Old and stored memories can become vulnerable if they are recalled (reactivated). These findings led to the hypothesis that when an old memory is reactivated it again becomes labile, and it does so in order to incorporate new information. This process of returning to a labile state after recall can be useful to develop therapeutic approaches for treating traumatic memories (traumatic stress disorders). We are working to understand which brain regions and molecular mechanisms underlie memory destabilization and re-stabilization after recall.

A clinically relevant model in which we apply these studies is addiction.. When drug addicts are exposed to cues that remind them of the rewarding state of the drug, they experience a strong craving response. This compulsive response seems to use mechanisms similar to those involved in memory formation. We are working on the identification and characterization of the molecular changes that occur in the brain when an addictive response is formed. Using rat models of conditioning to a drug of abuse (morphine), we aim at identifying which gene and protein are essential for making a brain addicted and which strategy we can use to disrupt this response. Areas of interest include: Learning and memory responses in vivo (behavior); Analysis of patterns of gene expression (gene arrays); temporally and anatomically restricted gene manipulation; memory reactivation, amnesia, addiction.

Visit Dr. Cristina Alberini's Neurobiology of Learning and Memory for more information.

Pollonini G, Gao V, Rabe A, Palminiello S, Albertini G, Alberini CM. Abnormal expression of synaptic proteins and neurotrophin-3 in the Down syndrome mouse model Ts65Dn. Neuroscience 2008; 156: 99-106.

Taubenfeld SM, Riceberg JS, New AS, Alberini CM. Preclinical Assessment for Selectively Disrupting a Traumatic Memory via Postretrieval Inhibition of Glucocorticoid Receptors. Biol Psychiatry 2008 Aug 16;.

Alberini CM. The role of protein synthesis during the labile phases of memory: revisiting the skepticism [review]. Neurobiol Learn Mem 2008; 89(3): 234-246.

Milekic MH, Pollonini G, Alberini CM. Temporal requirement of C/EBPbeta in the amygdala following reactivation but not acquisition of inhibitory avoidance. Learn Mem 2007 Jul 18; 14(7): 504-511.

Tronel S, Alberini CM. Persistent disruption of a traumatic memory by postretrieval inactivation of glucocorticoid receptors in the amygdala. Biol Psychiatry 2007 Jul 1; 62(1): 33-39.

Garcia-Osta A, Tsokas P, Pollonini G, Landau EM, Blitzer R, Alberini CM. MuSK expressed in the brain mediates cholinergic responses, synaptic plasticity, and memory formation. J Neurosci 2006 Jul 26; 26(30): 7919-7932.

Milekic MH, Brown SD, Castellini C, Alberini CM. Persistent disruption of an established morphine conditioned place preference. J Neurosci 2006 Mar 15; 26(11): 3010-3020.

Tronel S, Milekic MH, Alberini CM. Linking new information to a reactivated memory requires consolidation and not reconsolidation mechanisms. PLoS Biol 2005 Sep; 3(9): e293.

Alberini CM. Mechanisms of memory stabilization: are consolidation and reconsolidation similar or distinct processes? [review]. Trends Neurosci 2005 Jan; 28(1): 51-56.