Claudia Fallini

  • Assistant Professor
  • Phone: 401.874.4968
  • Email:
  • Office Location: SSRC, Rm 105


Dr. Fallini received her Ph.D. from the Università degli Studi di Milano (Italy) in 2009, where she gained interest in the basic cellular and molecular mechanisms leading to neurodegeneration. In particular she focused her studies on the role of mRNA regulation in the maintenance and function of motor neurons.

After she graduated, she moved to the US to start her postdoctoral training in the laboratory of Dr. Gary Bassell at Emory University (Atlanta, GA) first and Dr. Landers’ lab at UMASS Medical School (Worcester, MA) later. There, she continued to pursue her research interests and applied her skills to the study of the neurodegenerative diseases SMA and ALS/FTD, focusing on the role of the cytoskeleton in modulating mRNA metabolism and neuronal function.

Dr. Fallini joined URI and started her independent laboratory in the Fall 2019. Using human induced pluripotent stem cell models, she is investigating the interplay between the cytoskeleton and nuclear homeostasis in ALS and Alzheimer’s disease. These studies highlight the importance of the cytoskeleton in regulating basic cellular functions in neurons that are disrupted in disease.


The overarching goal of the Fallini Lab is to dissect the molecular and cellular changes that occur in postmitotic neurons during ageing and in pathological conditions, such as Amyotrophic Lateral Sclerosis, Frontotemporal Dementia (ALS/FTD) and Alzheimer’s Disease. Our current research is focused on investigating the crosstalk between the actin cytoskeleton, a regulator of cell morphology and structural integrity, and the nuclear pore, the master regulator of protein and RNA shuttling in and out of the nucleus. To investigate these questions, we have established patient-derived induced pluripotent stem cell (iPSC) culture and differentiation into human cortical and motor neurons, an exceptionally valuable and physiologically relevant system to study human disease in a dish. We have several ongoing projects:

  1. The role of the mechanosensitive pathway in the initiation and progression of ALS. Cells are tightly connected to their environment and very sensitive to changes in mechanical strain exerted on the cell from their surroundings. While these mechanisms are known to regulate cell differentiation and survival in dividing cells, little is known about their relevance to neuronal maintenance, particularly during aging.
  2. Analysis of transcriptional and proteomic changes in cortical and motor neurons carrying ALS-causing mutations. The nuclear and cytoplasmic compartments are characterized by wildly different protein composition. The maintenance of this compartmentalization depends on the functional integrity of the nuclear pore, the largest protein assembly in the cell. Disruption of nuclear pores has been recently identified as a key driver of disease in multiple neurodegenerative diseases. Our research aims at defining the downstream consequences of nuclear pore disruption on the nucleocytoplasmic distribution of regulatory proteins and the ability of neurons to modulate their transcriptional response to positive and negative stimulations.
  3. Ischemic stress impacts neuronal survival by altering nuclear pore function. Stroke is an established risk factor for Alzheimer’s disease, but the molecular mechanisms driving this link are unclear. Our research aims at defining the cellular consequences of acute ischemia that can set the stage for chronic neurodegeneration.


  • Ph.D. in Molecular Medicine, Università degli Studi (Milano, Italy), 2009
  • M.S. Degree in Medical Biotechnology, Università degli Studi (Milano, Italy), 2003

Selected Publications

D.M. Baron, A.R. Fenton, S. Saez-Atienzar, A. Giampetruzzi, A. Sreeram, Shankaracharya, P.J. Keagle, V.R. Doocy, N.J. Smith, E.W. Danielson, M. Andresano, M.C. McCormack, J. Garcia#, V. Bercier, L. Van Den Bosch, J.R. Brent, C. Fallini, B.J. Traynor, E.L.F. Holzbaur, J.E. Landers. ALS-associated KIF5A mutations abolish autoinhibition resulting in a toxic gain of function. Cell Reports (2022) Apr 5;39(1):110598

A. Giampetruzzi, E.W. Danielson, V. Gumina, M. Jeon, S. Boopathy, R.H. Brown, A. Ratti, J.E. Landers, C. Fallini. Modulation of actin polymerization affects nucleocytoplasmic transport in multiple forms of Amyotrophic Lateral Sclerosis. Nature Communications. (2019) 10(1):3827. PMID: 31444357

PG. Donlin-Asp, C. Fallini, J. Campos, CC. Chou, ME. Merritt, HC. Phan, GJ. Bassell, W. Rossoll. The Survival of Motor Neuron Protein Acts as a Molecular Chaperone for mRNP Assembly. Cell Reports. (2017) 14;18(7):1660-1673.

C. Fallini, P.G. Donlin-Asp1, J.P. Rouanet*, G.J. Bassell, W. Rossoll. Deficiency of the survival of motor neuron (SMN) protein impairs mRNA localization and local translation in the growth cone of motor neurons. Journal of Neuroscience (2016) 36(13):3811-20. * Undergraduate author

B.N. Smith*, N. Ticozzi*, C. Fallini*, A.S. Gkazi*, S. Topp*, K.P. Kenna, E.L. Scotter, J. Kost, P. Keagle, J.W. Miller, D. Calini, C. Vance, E.W. Danielson, C. Troakes, C. Tiloca, S. Al-Sarraj, E.A. Lewis, A. King, C. Colombrita, V. Pensato, B. Castellotti, J. de Belleroche, F. Baas, A. LMA ten Asbroek, P.C. Sapp, D. McKenna-Yasek, R.L. McLaughlin, M. Polak, S. Asress, J. Esteban-Pérez, J.L. Muñoz-Blanco, M. Simpson, SLAGEN Consortium,W. van Rheenen, F.P. Diekstra, G. Lauria, S. Duga, S. Corti, C. Cereda, L. Corrado, G. Sorarù, K.E. Morrison, K.L. Williams, G.A. Nicholson, I.P. Blair, P.A. Dion, C.S. Leblond, G.A. Rouleau, O. Hardiman, J.H. Veldink, L.H. van den Berg, A. Al-Chalabi, H. Pall, P.J. Shaw, M.R. Turner, K. Talbot, F. Taroni, A. García-Redondo, Z. Wu, J.D. Glass, C. Gellera, A. Ratti, R.H. Brown Jr., V. Silani, C.E. Shaw, J.E. Landers. Exome-wide Rare Variant Analysis Identifies TUBA4A Mutations Associated with Familial ALS. Neuron (2014) 84(2):324-31. doi: 10.1016/j.neuron.2014.09.027

C. Fallini, H. Zhang, Y. Su#, V. Silani, R. Singer, W. Rossoll, G.J. Bassell. The Survival of Motor Neuron (SMN) Protein Interacts with the mRNA-Binding Protein HuD and Regulates the Localization of Poly(A) mRNA in Primary Motor Neuron Axons. Journal of Neuroscience (2011) 31(10):3914-25