Dr. Daniele Bano
Group Leader
German Center for Neurodegenerative Diseases (DZNE)
Ludwig-Erhard-Allee 2
53175 Bonn
daniele.bano(at)dzne.de
+49 (0) 228 / 43302-510
More information
Areas of investigation/research focus
The unique features of the nervous system rely on the extensive and intricate interactions between different types of cells, which play a prominent role in shaping brain circuitry. In older humans, progressive changes of neuronal morphology and functional alteration of synaptic connectivity are key determinants of cognitive decline and brain disorders. Although the link between ageing and age-related brain pathologies is undeniable, the molecular mechanisms underlying the onset of neuronal dysfunctions still remains elusive.
In our laboratory, we aim to characterize new genes, which can affect ageing and can delay cognitive decline and neurodegenerative diseases.
Significance
- The nematode, a model for studying aging and neurodegeneration.
According to the World Health Organization, progress in medical care, together with improved nutrition and hygienic conditions, has resulted in a demographic shift of the population towards older ages. With the increasing proportion of older people in the population, the long term care of patients affected by age-related disorders, including Alzheimer’s and Parkinson’s disease, will be a major burden to our health care system. In humans, ageing is manifested by an overall decline in the tissue homeostasis and in the inability of the organism to respond adequately to environmental stress. In view of this functional decline, age is considered one of the major risk factors for the development of chronic diseases, including conditions particularly debilitating and without any clinical therapy. From this perspective, there is a great need to understand the nature of ageing and whether the onset of age-related disorders can be delayed. In the past, ageing was considered simply a process of slow deterioration promoted by accidental environmental stress. On the contrary, it is now evident that ageing is a biological process tightly regulated by evolutionary conserved molecular pathways.
Most of these programs involve signaling information from growth factors, nutrients, intracellular energy status and environmental cues, which can directly or indirectly alter the activity of intracellular sensors and, ultimately, cellular metabolism. Particularly interesting in this regard is the effect of some commercial drugs, such as rapamycin or resveratrol, on longevity, which further confirms that ageing can be modulated pharmacologically. Unfortunately, our understanding of the signaling pathways which promote lifespan extension is still elusive. Nevertheless, as the tuning of the same pathways that affect longevity can also delay brain pathologies, an attractive option emerges: we will likely be able to reduce the incidence of age-related disorders by tweaking ageing!
Approaches
We use the nematode Caenorhabditis elegans and transgenic mouse models to characterize new pathways that can extend lifespan. C. elegans is a short-lived animal, which allows us to perform cheap genetic screenings for modulators of longevity in a relatively short time. Mouse models are used to assess the relevance of our candidates on ageing and, more importantly, on neurodegenerative disorders. Molecular and cellular biology, together with genetic approach and fluorescent confocal microscopy analysis, are widely adopted as part of our routine work.
Publications
Calcium-Dependent Dephosphorylation of the Histone Chaperone DAXX Regulates H3.3 Loading and Transcription upon Neuronal Activation.
Michod D, Bartesaghi S, Khelifi A, Bellodi C, Berliocchi L, Nicotera P, Salomoni P. Neuron. 2012 Apr 12;74(1):122-35.
Neurodegenerative processes in Huntington's disease.
D Bano, F Zanetti, Y Mende, P Nicotera; Cell Death Dis. 2011 Nov 10;2:e228. doi: 10.1038/cddis.2011.112.
p73: a multifunctional protein in neurobiology.
R Killick, M Niklison-Chirou, R Tomasini, D Bano, A Rufini, F Grespi, T Velletri, P Tucci, BS Sayan, F Conforti, E Gallagher, P Nicotera, TW Mak, G Melino, RA Knight, M Agostini; Mol Neurobiol. 2011 Apr;43(2):139-46. Epub 2011 Mar 8.
Ageing, Neuronal Connectivity and Brain Disorders: An Unsolved Ripple Effect.
Bano D, Agostini M, Melino G, Nicotera P, Mol Neurobiol. 2011 Apr;43(2):124-30. Epub 2011 Jan 15.
p73 regulates maintenance of neural stem cell.
M Agostini, P Tucci, H Chen, RA Knight, D Bano, P Nicotera, F McKeon, G Melino; Biochem Biophys Res Commun. 2010 Dec 3.
Ryanodine receptor-2 upregulation and nicotine-mediated plasticity.
E Ziviani, G Lippi, D Bano, E Munarriz, S Guiducci, M Zoli, KW Young, P Nicotera; EMBO J. 2011 Jan 5;30(1):194-204. Epub 2010 Nov 26.
Nuclear pore complex during neuronal degeneration: cracking the last barrier.
Bano D., Hengartner M.O., Nicotera P. Nucleus 1:2; March/April 2010:136-138.
Alteration of nucleocytoplasmic transport in Ca2+-mediated neuronal demise.
Bano D., Dinsdale D., Cabrera-Socorro A., Maida S., Lambacher N., McColl B., Ferrando-May E., Hengartner M.O., Nicotera P. Cell Death and Differentiation 2010 Jan; 17(1):119-33.
Mitochondrial Ca2+ signalling in hippocampal neurons.
Young K.W., Bampton E., Pinon L., Bano D., Nicotera P. Cell Calcium 2007 Aug 29.
The plasma membrane Na+/Ca2+ exchanger is cleaved by distinct protease families in neuronal death.
Bano D., Munarriz E., Chen H.L., Ziviani E., Lippi G., Young K.W., Nicotera P. Ann N Y Acad Sci. 2007 Mar; 1099: 451-5
Ca2+ signals and neuronal death in brain ischemia.
Bano D., Nicotera P. Stroke 2007 Feb, 38 (2Suppl); 674-6
Ca2+ signals and death programmes in neurons.
Berliocchi L., Bano D., Nicotera P. Philos Trans R Soc Lond Biol Sci. 2005 Dec 29; 360(1464): 2255-8.
Calpain cleavage regulates the protein stability of p73.
Munarriz E., Bano D., Sayan A.E., Rossi M., Melino G., Nicotera P. Biochem Biophys Res Commun. 2005 Jun 20;333(3):954-960.
Cleavage of the Plasma Membrane Na+/Ca2+ Exchanger in Excitotoxicity.
Bano D., Young K.W., Guerin C.J., LeFeuvre R., Rothwell N.J., Naldini L., Rizzuto R., Carafoli E. and Nicotera P. Cell 2005 Jan 28: 120 (2): 275-285.