Pt(II)-based agents are used in approximately 50% of all cancers that are treated with chemotherapy. Unfortunately, the dose-limiting toxicity of these agents remains problematic for patients undergoing treatment. Additionally, Pt(II) therapeutics suffer from transporter-dependent uptake, limited chemical functionalization, and high susceptibility to inactivation by free thiols within the cytosol. Developing small molecules with non-canonical mechanisms of action is one strategy that can be employed to circumvent these limitations. Utilization of coordination complexes with Ru(II) metal centers is one attractive strategy. Ru(II) compounds are often octahedral, facilitating greater accessibility for chemical diversity; Ru(II) complexes use passive transport and transferrin-mediated transport for cellular uptake; Ru(II) is a harder Lewis acid than Pt(II), facilitating reduced thiol coordination, which results in reduced inactivation. Herein, we investigate several Ru(II) scaffolds that display non-canonical mechanisms. They are able to preferentially induce ribosome biogenesis stress and mitochondrial membrane uncoupling. Complementary to this work, we investigated the mechanism of action for photoactive chemotherapeutics (PACTs) and photodynamic therapeutics (PDTs). Despite the fact that reactive oxygen species (ROS) generated by PDTs can oxidize nucleobases, cellular bioenergetic pathways are effectively shut down before DNA damage could be recognized by DNA damage repair (DDR) machinery, suggesting that, unlike Pt(II) therapeutics, DNA damage is not the cause of cell death for these compounds.

"Transition-metal catalyzed Suzuki-Miyaura (SM) cross coupling is a powerful synthetic method for constructing carbon-carbon and carbon-heteroatom bonds in designing organic compounds, agrochemicals, pharmaceuticals, and precursors for materials.  However, the nature of catalysis and identity of the transition metal catalysts used in these reactions remain under debate or unknown. This work reports the studies of three metals: Pd, Cu, and Ni. Pd-nanocluster catalysts and their formation in ligand-free SM reactions with Pd(II) nitrate as a precatalyst was investigated. The catalysts are water-soluble neutral Pd tetramer and trimer in their singlet electronic states as identified by UV-Vis absorption spectroscopy and are formed by leaching of spherical Pd(0) nanoparticles with an average diameter of about three nanometers. The Pd(0) nanoparticles are produced by reducing Pd(II) nitrate and characterized with transmission electron microscopy (TEM) and Pd-K edge extended x-ray fine structure spectroscopy (EXAFS). The Pd(II) reduction is induced by ethanol and enhanced by potassium hydroxide and monitored with x-ray photoelectron spectroscopy (XPS). For the Cu-catalyzed SM coupling, a water-soluble active molecular catalyst, and its formation in the ligand-free SM cross-coupling reactions with copper iodide as the precatalyst in aqueous solutions has been reported. The SM coupling is homogeneous in nature, and the molecular catalyst is Cu(OH) in its singlet electronic state also identified by experimental and computational UV-Vis absorption spectroscopy. The Cu(OH) catalyst is generated through the leaching of oval-shaped Cu₂O nanoparticles, which are characterized with X-ray Auger electron spectroscopy, X-ray absorption spectroscopy (XAS), and TEM. The soluble Cu(OH) species is stable for at least four weeks under ambient conditions. Similarly, for Ni-catalyzed ligand-free SM coupling, the active Ni catalyst is reported as Ni(0) species with Ni(0) powder as the precatalyst. The SM coupling is also homogeneous in nature. The water-soluble active Ni(0) catalyst is generated through the leaching of Ni(0) nanoparticles, which are characterized with XPS, XAS, and TEM. The water-soluble active Ni(0) catalyst species is stable for at least eight weeks under ambient conditions. Thus, this talk showcases the nature of catalysis and the identity of catalytically active species in ligand-free SM reactions catalyzed by Pd, Cu, and Ni transition metals."

Transition metals such as Fe, Cu, and Zn are micronutrients that have critical roles at the host-pathogen interface as both the host and pathogen need them for survival. The host has developed innate immune strategies to sequester metals such as Fe which pathogens need for survival as well as strategies to secrete certain metals such as Cu to exert toxic effects on the pathogen. In return, pathogens have evolved strategies to scavenge metals they need, as well as export or store excess metal. Candida albicans, is an opportunistic fungal pathogen that has the capacity to cause systemic infections that can lead to death in immunocompromised and immunosuppressed populations. Azoles, such as fluconazole, are one of the four classes of antifungals that are FDA approved and are a first line treatment for C. albicans infections.  Our lab has shown significant changes to metallohomeostasis of C. albicans as a result of fluconazole treatment. In this talk, I will discuss our work to determine how C. albicans overcomes azole treatment by modifying Cu homeostasis pathways. I will also discuss a potential strategy that focuses on metal dyshomeostasis and takes advantage of our innate immune system to develop a possible treatment for C. albicans infections.

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1:30-1:50 PM:  Prof. Fabio Di Domenico: Department of Biochemical Sciences “A. Rossi-Fanelli” - Sapienza University of Rome

Title: “Protein O-GlcNAc modification in the central nervous system: from nutrient sensing to the development of Alzheimer disease signatures.”

Abstract: Protein O-GlcNAc modification is a dynamic non-canonical form of protein O-Glycosylation considered a rheostat of cellular reprogramming under differential metabolic conditions. Alterations of nutrient availability in the brain, as observed in Alzheimer Disease and in other neurodegenerative disorders, lead to aberrant O-GlcNAc levels and trigger the development of neuropathological signatures. We analyzed by proteomics approaches the total and protein-specific levels of O-GlcNacylation, the O-GlcNAc cycling and the development of AD signatures in mouse models of both AD-like dementia (DS mice) and metabolic disease (high fat diet mice). Data on DS mice supported the presence of altered hippocampal O-GlcNAc levels and their implications in the AD-related neurodegenerative process. Accordingly, metabolic defects observed in high fat diet (HFD) mice promoted the impairment of protein O-GlcNAcylation, eventually resulting in mitochondrial defects, reduced energy consumption and in the development of AD signatures. By testing the effects of the O-GlcNAcylation inducer Thiamet-G to rescue brain alterations and AD development, we demonstrated its beneficial effect on cognition associated with the recovery of O-GlcNAc levels of protein belonging to key functional pathways, such as, neuronal architecture, stress response mechanisms and energy production. Our studies clarified the molecular mechanisms by which reduced protein O-GlcNAcylation promote the progression of brain pathology, thus laying the foundations to understand the main processes linking metabolic defects and neurodegenerative processes

Bio: Fabio Di Domenico is Full professor of Biochemistry at Sapienza University of Rome. He obtained his PhD degree in Biochemistry in 2009. Before gaining his current position, he performed his research under the supervision of Prof. Butterfield at University of Kentucky, where he has been involved in the application of redox proteomics to brain samples from Alzheimer patients. His research is currently focused in understanding the mechanisms that associates the alteration of protein homeostasis with the development of Alzheimer-like dementia. Collected data from his laboratory postulate that aberrant proteostasis, observed in both Alzheimer and Down syndrome patients, is strictly associated with the increase of oxidative damage as result of compromised antioxidant response and faulty protein degradative systems. Recently, his studies revealed that the reduction a nutrient sensing protein post translational modification, O-GlcNAc, might represents a key molecular link between metabolic defect and the development of Alzheimer Disease signatures.

1:50-2:10 PM: Prof. Eugenio Barone: Sapienza University of Rome

Title: “Insulin signaling alterations impair mitochondrial bioenergetics in the brain: identification of a novel molecular mechanism linking metabolic and neurodegenerative diseases.”

Abstract: Brain insulin signaling acts as a key regulator for gene expression and cellular metabolism, both events sustaining neuronal activity and synaptic plasticity mechanisms. Alterations of this pathway, known as brain insulin resistance, are associated with an increased risk of developing age-related cognitive decline and neurodegeneration. Studies from our group and in collaboration with Dr. Butterfield's group uncovered the role of the enzyme biliverdin reductase A (BVRA) that, beyond its activity in the degradation pathway of heme, is a novel regulator of the insulin signaling. BVRA is a direct target of the insulin receptor (IR), similar to the insulin receptor substrate-1 (IRS1). IR phosphorylates BVRA on specific Tyr residues and activates BVRA to function as a Ser/Thr/Tyr kinase. Moreover, downstream from IRS1, BVRA works as a scaffold protein favoring: the translocation of GLUT4-containing vesicles to the plasma membrane (to increase glucose uptake in response to insulin), the AKT-mediated inhibition of GSK3β (that promotes cell survival) and the AMPK-mediated inhibition of MTOR (that is involved in autophagy). Moreover, we recently discovered that BVRA regulates mitochondrial bioenergetics in response to insulin, thus supporting cell metabolism. Ground-breaking findings from our group revealed that oxidative stress-induced impairment of BVRA is a key event driving insulin resistance development either in the brain or in peripheral tissues. Conversely, rescuing BVRA activity reduces oxidative stress levels and ameliorate brain insulin signaling activation, both events contributing to improved cognitive functions in animal models of neurodegeneration.  Overall, our data suggest that dysfunctions of BVRA are responsible for increased oxidative stress levels and the impairment of insulin signaling. Alterations of BVRA also impair energy metabolism thus contributing to create a harmful synergistic effect triggering the development of neurodegeneration.   

Bio: Graduated in Pharmaceutical Chemistry and Technology in 2006 and got a PhD in Neuroscience in 2011. The overarching goal of his laboratory is to clarify the link between defects of neurotrophic signaling (insulin and GLP1) and increased cell damage during ageing and neurodegeneration. During the last years his research also focused on Down syndrome demonstrating for the first time that brain insulin resistance develops very early in DS, independently of peripheral alterations [Neurobiol Dis (2020); Free Rad Biol Med (2021); Alzheimer’s and Dementia (2021)].  Dr. Barone authored 92 publications, most of which dealing with the role of oxidative stress in neurodegenerative disorders, i.e., Alzheimer disease and DS. He was recipient of prestigious grants from the Alzheimer Association (2020-24), Jerome Lejeune Foundation (2019-21 and 2022-24), European Commission (2014-16) and Italian Ministry of Research (2015-18), among the others. Dr. Barone was one of the firsts two recipients of the SFRBM fellowship Awards (2010) while he was a visiting PhD student in the lab of Dr. Allan Butterfield at the University of Kentucky, and recipient of many international awards including those from:  SFRBM (2015 and 2016), EPHAR (2013), AAIC (2017) and T21RS (2017). In 2021 he was appointed as co-chair for the European Brain Research Area (EBRA) for the Trisomy 21 cluster. He serves as chair of the Strategic Alliances & Outreach Committee of the SfRBM and the chair of the Sponsoring and Membership Committee of the T21RS.

2:10-2:30 PM: Dr. Antonella Tramutola: Department of Biochemical Sciences - Sapienza University of Rome

Title: “Intranasal insulin administration ameliorates learning and memory deficits by rescuing protein oxidative stress damage in Alzheimer disease.”

Abstract: Brain insulin resistance (bIR) heavily impacts on the core pathological processes of aging and Alzheimer disease (AD) since insulin regulates brain metabolism and cognitive functions. A close link among bIR, oxidative stress (OS) and mitochondrial defects exists, that contributes to brain dysfunctions observed in AD. Intriguingly, several studies suggest that intranasal insulin (INI) administration enhances cognitive performances and reduced AD neuropathology both in humans and animal models of neurodegeneration. We focused on the interplay between OS and bIR, by testing the hypothesis that rescuing brain insulin signaling activation by the mean of INI results in improved mitochondrial functions and reduced OS-induced damage to proteins and lipids in the brain of 3xTg-AD mice (a model of AD).

Methods. 12-month-old 3×Tg-AD and wild-type (non-Tg) mice were treated with INI (2 UI) or vehicle (saline) every other day for 2 months. At the end of the treatment mice underwent cognitive tests and then sacrificed to collected brain samples for biochemical analyses. Insulin signaling pathway and OS marker levels, i.e., PC, 4-HNE and 3-NT were evaluated in the frontal cortex. A redox proteomics approach was used to identify specific protein targets of 3-NT modifications. Mitochondrial functions were evaluated by measuring mitochondrial complexes (OXPHOS) protein levels and activities.

Results and Conclusions. INI administration led to a significant improvement of cognitive functions along with an amelioration of insulin signaling activation and reduced OS levels in 3xTg-AD mice. In particular, a consistent reduction of 3-NT levels was observed. Redox proteomics allowed to identify several proteins with reduced 3-NT modifications, that belong to key pathways, such as protein degradation and energy metabolism, known to be involved in the progression of AD. Remarkably, reduced 3-NT levels on mitochondrial proteins were responsible for the observed improvement of mitochondrial activity and brain energy metabolism in 3xTg-AD mice. We propose that INI represents a promising approach to reduce proteins OS-induced damage and restore mitochondrial bioenergetics in AD brain.

Bio: Antonella Tramutola is Assistant Professor of Biochemistry at the Department of Biochemical Sciences at Sapienza University of Rome. She obtained her PhD in Neuroscience at the Catholic University School of Medicine in Rome. In 2014, she spent 1 year as visiting researcher at Department of Chemistry at the University of Kentucky hosted by Professor D. Allan Butterfield. Her research is focused on exploring the role of the proteostasis network in neuronal death in Alzheimer Disease (AD) and Down Syndrome (DS), as they share common pathological hallmarks. She is examining the dysfunction of components of the protein quality control system, caused by oxidative damage, and the pathways involved in proteostasis such as mTOR signaling, the insulin cascade, and the autophagy-proteasome system. Through studying post-mortem brain tissue, cell culture, and animal models of AD or DS, her research is aimed at identifying common and divergent mechanisms of neurodegeneration. This could lead to investigating how these pathways could be targeted therapeutically to prevent neurodegenerative phenomena in DS and AD.

2:30-3:00 PM:  Questions and Answers Period for all three speakers

Abstract: The human cytochrome P450 1B1 (CYP1B1) is an emerging target for small- molecule therapeutics. Several solid tumors overexpress CYP1B1 to the degree that it has been referred to as a universal tumor antigen. Conversely, its expression is low in healthy tissues. CYP1B1 may drive tumorigenesis through promoting the formation of reactive toxins from environmental pollutants or from endogenous hormone substrates. Additionally, the expression of CYP1B1 in tumors is associated with resistance to several common chemotherapies and with poor prognoses in cancer patients. However, inhibiting CYP1B1 with small molecules has been demonstrated in cellular and murine model systems to reverse this resistance phenotype. Thus, an approved CYP1B1 inhibitor may be of immense benefit to cancer patients struggling against chemotherapy-resistant disease.

However, developing selective inhibitors of CYP1B1 is challenging due to the existence of approximately fifty related cytochromes P450 found in humans which share similar structural features. Confounding this fact, CYP1B1 preferentially binds substrates of low three-dimensional complexity and with high lipophilicity, which from a synthetic viewpoint are relatively nondescript, making rational inhibitor design difficult.

This work offers new synthetic approaches toward the solution to the challenge of developing selective CYP1B1 inhibitors. The first part of the work describes the discovery and mode of action of a previously unknown inhibitor of CYP1B1 active at sub-nanomolar concentrations, and with unprecedented selectivity compared to existing inhibitors. Next, the pharmacokinetic optimization of this lead compound was undertaken resulting in an improved lead with excellent metabolic stability for future applications in disease models, and with the long-term goal of translation into the clinic for use in human patients. Together, the development of a series of new molecular entities is described which enable the exquisite control of the activity of this medically relevant enzyme and is an important step toward the development of drug candidates.

Abstract: In this seminar, we will focus on our recent work on two different thin film systems – metal halide perovskites and organic semiconductors.For one, through proper control of processing, we are able to realize pinhole free organic semiconductor films with single crystal grains with mm dimensions. We have found that transport in these films is considerably improved compared to disordered films, and that organic solar cells incorporating these long-range-ordered films exhibit highly delocalized, and band-like charge transfer (CT) states, contributing to noticeably lower energy losses. We will discuss these aspects and our understanding to-date of which molecules are amenable to the formation of such films, and how to propagate their growth. Also, organic hole transport materials (HTMs) are ubiquitous in halide perovskite solar cells, but what is less well known is that shallow HTMs that facilitate hole extraction from the perovskite also enable halogen transport. We will present our understanding of this phenomenon, as well as impacts to devices with regard to Au diffusion.

Bio: Barry Rand earned a BE in electrical engineering from The Cooper Union in 2001. Then he received MA and PhD degrees in electrical engineering from Princeton University, in 2003 and 2007, respectively. From 2007 to 2013, he was at imec in Leuven, Belgium, ultimately as a principal scientist, researching the understanding, optimization, and manufacturability of thin-film solar cells. Since 2013, he is in the Department of Electrical Engineering and Andlinger Center for Energy and the Environment at Princeton University, currently as a Professor. Prof. Rand’s research interests highlight the border between electrical engineering, materials science, chemistry, and applied physics, covering electronic and optoelectronic thin-films and devices. He has authored over 160 refereed journal publications, has 25 issued US patents, and has received the 3M Nontenured Faculty Award (2014), DuPont Young Professor Award (2015), DARPA Young Faculty Award (2015), and ONR Young Investigator Program Award (2016).

Dr. Shanina Sanders Johnson
Ph.D., University of North Carolina at Chapel Hill
B.S., Hampton University
At Spelman since 2011, promoted to Associate Professor recently

Abstract: Dr. Johnson's work has involved implementing culturally relevant pedagogies into organic chemistry lecture and laboratories. Activities that provide context to chemistry have been created and implemented to allow for incorporation of student background, interests, and experiences into the curriculum. These strategies allow students to see the relevance of science, reflect on their science identity, and connect their personal experiences and knowledge to their learning. Additionally, allowing for cultural context in the curriculum supports diversity within the classroom on multiple levels. This type of strategy is ultimately aimed at not only diversifying chemistry but also ushering in social change that provides for a more equitable field.  

Abstract: Halide perovskites are exciting new semiconductors that show great promising in low cost and high-performance optoelectronics devices including solar cells, LEDs, photodetectors, lasers, etc. However, the poor stability is limiting their practical use. In this talk, I will present the development of a new family of stable organic-inorganic hybrid electronic materials, namely, Organic Semiconductor-Incorporated Perovskites (OSiP). Energy transfer and charge transfer between adjacent organic and inorganic layers are extremely fast and efficient, owing to the atomically-flat interface and ultra-small interlayer distance. Moreover, the rigid conjugated ligands dramatically enhance materials’ chemical stability and suppresses solid-state ion diffusion and electron-photon coupling, making them promising for many applications. Based on this, we demonstrate for the first time an epitaxial halide perovskite heterostructure with near atomically-sharp interface, which pave the way for perovskite nanoelectronics and nanophotonics. Finally, using this stable and solution-processable OSiPs, we demonstrate the fabrication of high-quality thin films, which enable highly stable and efficient solar cells and LEDs.

Bio: Dr. Letian Dou is currently the Charles Davidson Associate Professor of Chemical Engineering at Purdue University. He obtained his B.S. in Chemistry from Peking University in 2009 and Ph.D in Materials Science and Engineering from UCLA in 2014. From 2014 to 2017, he was a postdoctoral fellow at the Department of Chemistry, University of California-Berkeley and Materials Science Division, Lawrence Berkeley National Laboratory. His research interest includes the design and synthesis of organic-inorganic hybrid materials and low-dimensional materials, fundamental understanding of the structure-property relationships, as well as applications in high performance electronic and optoelectronic devices. He is a recipient of AIChE Owens Corning Early Career Award (2022), NSF CAREER Award (2021), Advanced Materials Rising Stars Award (2021), Office of Naval Research Young Investigator Award (2019), Highly Cited Researcher in Cross-Fields (2019-2022), MIT Technology Review Innovators Under 35-China Award (2018), and MRS Graduate Student Award (2014).

Abstract: Supramolecular gelation is a fascinating self-assembly process that closely mimics important natural and biological events. The supramolecular nature of such materials imparts the system with reversibility and adaptivity. The individual or collective contributions of various non-covalent interactions, such as hydrogen bonding, π– π stacking, metal–ligand coordination, host–guest interactions, and van der Waals interactions, are at the focal point of the structural evolution during an assembly process. Supramolecular gels have been studied extensively in the last few decades, mostly by exploiting the functional outputs for technological and medicinal applications. In comparison, pure structural investigations of supramolecular gel materials are rather limited. The lack of convincing structural data has multiple implications. The two most crucial factors for structural investigations are the experimental time scale and the sensitivity of the measurements towards structural evolution. Herein, we will investigate self-assembly processes of supramolecular nanoassmeblies under ambient versus non-ambient conditions. Specifically, we will probe how real-time measurements give valuable insights about nucleation and self-assembly of materials. The information obtained yields valuable information about structure-function correlation of materials which could have applications in several areas, including pharmaceutics and personal care. 

Bio: Dr. Harshita Kumari, is an Associate Professor in the Division of Pharmaceutical Sciences at University of Cincinnati. Dr. Kumari’s work in the area of solution chemistry of supramolecular complexes is widely recognized. She integrates neutron scattering with supramolecular chemistry to unravel structural altercations in solution.

Her current research focuses on integrating principles of modern biophysics into material and formulation science towards the development of novel skin care, oral care and hair care products. Her research projects focus on understanding mechanisms of delivery and deposition of actives onto the skin/hair and elucidating the parameters to control them. In addition, her research focuses on developing methods to construct novel nanometric delivery vehicles, based on the principles of self-assembly and molecular recognition. Her work is published in several peer reviewed journals.

Speakers
	Prof. Barry Halliwell National University of Singapore D. Phil. (Oxford), D. Sc. (London) Chairman, BMRC Advisory Council (BMAC), Agency for Science, Technology & Research (A*STAR) Distinguished Professor, Department of Biochemistry , National University of Singapore (NUS) Senior Advisor, Academic Appointments and Research Excellence, Office of the Senior Deputy President and Provost, NUS Program Leader, Neurobiology Research Program, Life Sciences Institute Professor Halliwell graduated from Oxford University with BA (first class honours) and D.Phil degrees. He holds a Doctor of Science degree from the University of London. He was a faculty member with King’s College London (1974-2000) and held a prestigious Lister Institute Research fellowship. He was a Visiting Research Professor of Internal Medicine and Biochemistry at the University of California Davis (1995-1999). He now holds several key positions in Singapore, as indicated above. Professor Halliwell is recognized for his seminal work on the role of free radicals and antioxidants in biological systems, being one of the world’s most highly-cited researchers with a Hirsch-Index of 168 (Based on Scopus, Jan 2023). His Oxford University Press book with John Gutteridge, Free Radicals in Biology and Medicine, now in its fifth edition (2015), is regarded worldwide as an authoritative text. He was honored as a Citation Laureate (2021) for pioneering research in free-radical chemistry including the role of free radicals and antioxidants in human disease. The distinction is awarded by Clarivate to researchers whose work is deemed to be of “Nobel Class” as they are among the most influential, even transformative, in their fields. He was one of 16 scientists (only three in Chemistry) listed in the 2021 Hall of Citation Laureates. Group Page 1 Group Page 2
	Prof. Marzia Perluigi Sapienza University of Rome Marzia Perluigi, PharmD, Ph.D., Head of Laboratory of Redox Biochemistry in Neuroscience (LRBN). Professional appointments: Professor of Biochemistry, Department of Biochemical Sciences “A. Rossi Fanelli" – Medical School Sapienza University of Rome. Fields of Expertise: Biochemistry and cell biology. The major research interest is the study of the role of oxidative stress in Down Syndrome (DS) and Alzheimer Disease (AD). Projects involve both the analysis of post-mortem brains, biological fluids, and cellular and animal models of the diseases. Current projects focus on defects of energy metabolism, failure of protein quality control (UPS and autophagy), impairment of mitochondrial activity, both in DS and AD. Further, preclinical studies are ongoing to test the neuroprotective effects of selected compounds able to prevent/slow the onset of dementia. Group Page
	Prof. Mark Mattson Johns Hopkins University Mark Mattson is the former Chief of the Laboratory of Neurosciences at the National Institute on Aging and is now on the faculty of Neuroscience at Johns Hopkins University School of Medicine. His research has advanced an understanding of the cellular signaling mechanisms that control the formation and plasticity of neuronal networks in the brain, and cellular and molecular mechanisms of brain aging and neurodegenerative disorders. His research has also elucidated how the brain responds adaptively to challenges such as fasting and exercise, and he has used that information to develop novel interventions to promote optimal brain function throughout life. Dr. Mattson is among the most highly cited neuroscientists in the world with more than 900 publications and 200,000 citations. He was elected a Fellow of the American Association for the Advancement of Science and has received many awards including the Metropolitan Life Foundation Medical Research Award and the Alzheimer’s Association Zenith Award. Mattson is the author of the book "The Intermittent Fasting Revolution: The Science of Optimizing Health and Enhancing Performance."

On Thursday, April 20th, the day before the Naff Symposium, the Chemistry Department also is hosting a Roundtable seminar involving three Department of Biochemistry faculty members from the Sapienza University of Rome, all of whom do research on Alzheimer disease and Down syndrome (persons with DS nearly always exhibit Alzheimer disease neuropathology in brain and dementia later in life).  Prof. Marzia Perluigi, one of our Naff Symposium presenters, also is from the Department of Biochemistry at the Sapienza University of Rome. This Roundtable seminar will begin at 1:30 pm in CHEM-PHYS Room 114 with a Q&A session from 2:30-3:00 pm.

Click here for more information about the event.

2023 Naff Symposium Committee

Prof. Allan Butterfield - (Chemistry) [Chair]

Prof. Marcelo Guzman - (Chemistry)

Prof. Daret St. Clair - (Toxicology/Cancer Biology)