Cell line-specific modulation of inflammation by oestradiol in an in vitro model of antenatal depression Madeline Kirkpatrick, Silvia Alboni, Federico Imbeni, Nicole Mariani, Nuriza Tukiran, Erin Mason-White, Carmine M. Pariante, Alessandra Borsini Brain Behavior and Immunity, 2026 Antenatal depression is linked to adverse neurodevelopmental outcomes in offspring, likely mediated by a multitude of biological mechanisms, including elevated maternal cytokines. However, factors modulating fetal vulnerability or resilience to inflammatory exposure remain unclear. This study examines whether the steroid hormone, oestradiol, can modulate inflammatory responses in an in vitro model of hippocampal neurogenesis, using two fetal hippocampal progenitor cell lines: female-derived HPC0A07/03C and male-derived HIP-009. Cells were pre-treated with oestradiol for 24- and 48-hours during proliferation, followed by interleukin-1beta (IL-1β) exposure prior to the initiation of differentiation. Markers of proliferation and neurogenesis, as well as inflammatory cytokines and kynurenine pathway metabolites, were assessed. In female HPC0A07/03C cells, oestradiol pre-treatment prevented IL-1β-induced proliferation and apoptosis, and reduced cytokine production. Conversely, in male HIP-009 cells, oestradiol pre-treatment did not prevent IL-1β-induced reduction of proliferation and apoptosis and indeed enhanced inflammatory responses after 48 h. In terms of differentiation, IL-1β produced opposite effects on neurogenesis across cell lines, increasing neuronal maturation in female HPC0A07/03C cells, but decreasing neurite complexity in male HIP-009 cells. Notably, oestradiol pre-treatment in both lines reduced neuronal differentiation and increased kynurenine levels, suggesting potentially detrimental long-term effects. These results highlight complex, potentially cell-line-dependent, sex-specific hormone-immune interactions shaping fetal neurodevelopment and underscore the need to investigate these interactions when assessing risks and developing therapeutic interventions for inflammation-related neurodevelopmental disorders.
Microbiota-gut-brain axis dysregulation in Alzheimer’s disease and its modulation through probiotic supplementation Moira Marizzoni, Elisa Mombelli, Silvia Alboni, Melissa Rosa, Davide Vito Moretti, Peppino Mirabelli, Luigi Coppola, Delia Luongo, Dominic Salamone, Samantha Saleri, Fabrizio Piazza, Veronica Begni, Marco Salvatore, Giovanni B. Frisoni, Annamaria Cattaneo Brain Behavior and Immunity, 2026 BACKGROUND: The microbiota-gut-brain axis (MGBA) has been implicated in the pathophysiology of Alzheimer's Disease (AD).Probiotics reduced the progression of ADin different mouse models, possibly through MGBA modulation, but human data are still limited. OBJECTIVE: Here, we evaluated whether differences in the gut microbiome (GM), pro-inflammatory markers and other MGBA mediators were associated with probable AD (pAD). We also assessed the impact of a 12-week probiotic treatment on MGBA. METHODS: Forty-five pAD patients and 47 healthy subjects (HC) were recruited at IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli of Brescia (Italy). An uncontrolled clinical investigation was performed to test the effects of 12-week probiotic supplementation in the pAD group. Fecal microbiota composition, intestinal and blood inflammatory markers, and microbiota-related metabolites were assessed before supplementation in all participants and after only in pAD. RESULTS: pAD patients showed intestinal inflammation, an altered GM profile, blood changes in the tryptophan metabolism, and reduced glutamate levels compared with HC (p-value < 0.049). Probiotic supplementation partially modulated these alterations, determining a reduction in several pro-inflammatory mediators, and an increase of GM-related protective factors, such as butyrate (p-value < 0.040) in pAD. CONCLUSIONS: These findings confirmed the presence of MGBA alterations in AD and suggested a potential beneficial effect of probiotic supplementation through modulation of GM functionality rather than composition. Further research is required to confirm these results and their clinical relevance.
The dietary ligands, omega-3 fatty acid endocannabinoids and short-chain fatty acids prevent cytokine-induced reduction of human hippocampal neurogenesis and alter the expression of genes involved in neuroinflammation and neuroplasticity Gargi Mandal, Silvia Alboni, Nadia Cattane, Moira Marizzoni, Samantha Saleri, Nikita Arslanovski, Nicole Mariani, Madeline Kirkpatrick, Annamaria Cattaneo, Carmine M. Pariante, Alessandra Borsini Molecular Psychiatry, 2025 The dietary ligands, omega-3 fatty acid endocannabinoids (eCBs) eicosapentaenoyl ethanolamide (EPEA) and docosahexaenoyl ethanolamide (DHEA), and short-chain fatty acids (SCFAs) acetate, propionate and butyrate, have anti-inflammatory and antidepressant properties. However, the molecular mechanisms underlying their action in the human brain remain elusive. Here, we treated human hippocampal neurons (HPC0A07/03 C) with eCBs (EPEA (300 pM) or DHEA (700 pM)), or SCFAs (acetate (200 uM), propionate (30 uM), butyrate (20 uM)), followed by interleukin (IL)1β (10,000 pg/ml) or IL6 (50 pg/ml). We found that treatment with either eCBs or SCFAs prevented IL1β- and IL6-induced reduction in neurogenesis and increase in apoptosis. These effects were mediated by IL1β-induced production of IL6, interferon-gamma (IFNγ) and tumour necrosis factor-alpha (TNFα), and by IL6-induced IL1β, IL8 and IL13, all of which were prevented by treatment with eCBs. In contrast, IL1β-induced production of IL6, IL12 and fractalkine (CX3CL1), and IL6-induced production of CX3CL1, were prevented by SCFAs. Treatment with IL1β and IL6 also increased the production of candidate kynurenine pathway metabolites, such as kynurenine (KYN) and nicotinic acid (NICA), which again were prevented by eCBs and SCFAs. We then conducted mRNA sequencing analysis to investigate cellular genes and signalling pathways relevant for the neuro-inflammatory changes previously observed, and putatively prevented by eCB and SCFA treatment. We found that IL1β decreased the expression of the neuroplasticity gene, FRY microtubule binding gene (FRY), and increased the expression of the neuroinflammation gene, U3 small nucleolar ribonucleoprotein homolog C subunit processome component (UTP14C), and both these effects were prevented by either acetate or propionate. Similarly, the expression of the proinflammatory gene, ADAM metallopeptidase with thrombospondin type 1 motif 1 (ADAMTS1), was increased by IL6, an effect that was prevented by either EPEA or acetate. Altogether, we identify novel anti-inflammatory and neurogenic mechanisms mediating the effect of eCBs and SCFAs on human hippocampal neurogenesis, which can be significant as potential future treatment candidates in the context of neuropsychiatric disorders.
Unraveling lipopolysaccharide-induced behavioral and molecular effects in Lymnaea stagnalis, an emerging model organism for translational neuroscience Veronica Rivi, Giovanna Rigillo, Silvia Alboni, Joris M. Koene, Luca Pani, Ken Lukowiak, Fabio Tascedda, Johanna M.C. Blom, Cristina Benatti International Immunopharmacology, 2025 In this study, we employed a reductionist (yet not simplistic) approach utilizing the established invertebrate model system of the pond snail, Lymnaea stagnalis , to investigate the behavioral and molecular effects of systemic administration of lipopolysaccharide (LPS)—a bacterial endotoxin—on the snails' central ring ganglia. Snails received injections of either a low dose (2.5 μg) or a high dose (25 μg) of LPS, and their behavioral and molecular responses were assessed at 2, 6, and 24 h post-injection. With the high dose, snails exhibited a significant increase in homeostatic aerial respiration lasting for at least 24 h, consistent with a sickness-like state induced by the immune challenge. Additionally, we found that when administered 2, 6, or 24 h before operant conditioning training, the high dose of LPS, impaired memory formation. To further explore the underlying molecular mechanisms, we examined the transcriptional effects of the two doses of LPS in the snails' central ring ganglia. Our analysis showed a dose- and time-dependent upregulation of immune and stress-related genes, including key enzymes involved in the kynurenine pathway (KP), toll-like receptor 4 (TLR4), and heat shock protein 70 (HSP70). Metabolomic analysis suggested that the high LPS dose shifted KP metabolism toward the production of neurotoxic metabolites within the ganglia, indicating a LPS-induced neuroinflammatory state. Together, our findings provide valuable insight into the conserved mechanisms of neuroinflammation in this invertebrate model, offering a simplified yet effective tool to further explore the molecular interactions between the immune and central nervous systems. • Lymnaea stagnalis was used to study behavioral and molecular effects of LPS. • High-dose LPS increased aerial respiration, indicating a sickness-like state. • LPS impaired learning and memory, mirroring effects seen in mammals. • LPS upregulated immune and stress genes in snail's central ring ganglia. • High-dose LPS shifted kynurenine metabolism toward neurotoxic metabolites in ganglia.
Targeted Metabolomics for the Analysis of p-Cresol in Mouse Brain: Impact of Biological Sex and Strain Laura Bertarini, Federico Imbeni, A. Vilella, Silvia Alboni, Federica Pellati ACS Chemical Neuroscience, 2025 p-Cresol, an environmental contaminant and endogenous metabolite derived primarily from the conversion of l-tyrosine by intestinal microflora, is gaining increasing attention, due to its potential impact on human health. Recent studies have highlighted elevated levels of p-cresol and its metabolites, including p-cresyl sulfate and p-cresyl glucuronide, in various populations, suggesting a correlation with neurodevelopmental and neurodegenerative conditions. While the role of this compound as a uremic toxin is well established, its presence and concentration within the central nervous system (CNS) remain largely unexplored. To address this gap, an high-performance liquid chromatography-electrospray ionization-tandem mass spectrometry (HPLC-ESI-MS/MS) method was optimized and validated for the first time in this work for the targeted metabolomics of p-cresol in brain tissues. This method enabled the quantification of this compound in different brain areas of adult male and female C57BL/6J mice and in the cortex of various mouse strains, including CD-1 and the idiopathic autism model BTBR T+Itpr3tf/J. Additionally, preliminary analyses of human cortex samples confirmed the presence of p-cresol, suggesting its relevance in human brain health. Moreover, metabolomic analyses have further explored the correlations between p-cresol and neurotransmitters, with a particular focus on dopaminergic and noradrenergic pathways. These findings pave the way for understanding the potential impact of p-cresol on neurochemical networks and its implications for neurodevelopmental and neurodegenerative disorders.
Female mice exhibit similar long-term plasticity and microglial properties between the dorsal and ventral hippocampal poles Eleonora De Felice, Bianca Caroline Bobotis, Giovanna Rigillo, Mohammadparsa Khakpour, Elisa Gonçalves de Andrade, Cristina Benatti, Antonietta Vilella, Fabio Tascedda, Cristina Limatola, Marie-Ève Tremblay, Silvia Alboni, Laura Maggi Brain Behavior and Immunity, 2025 The hippocampus is a heterogenous structure that exhibits functional segregation along its longitudinal axis. We recently showed that in male mice, microglia, the brain's resident immune cells, differ between the dorsal (DH) and ventral (VH) hippocampus, impacting long-term potentiation (LTP) mainly through the CX3CL1-CX3CR1 signaling. Here, we assessed the specific features of the hippocampal poles in female mice, demonstrating a similar LTP amplitude in VH and DH in both control and Cx3cr1 knock-out mice. In addition, the expression levels of Cx3cr1 and Cx3cl1 mRNA do not differ between the two poles in control mice. These data support the critical role of the CX3CL1-CX3CR1 signaling in setting the physiological amount of plasticity, equally between poles in females. Although BDNF is higher in DH compared to VH, the expression levels of inflammatory markers involved in plasticity and of phagocytosis markers in microglia are comparable between the two poles. In accordance, microglia soma and arborization area/perimeter, and microglial ultrastructure are similar across regions, with the exception of microglial density, cells arborization solidity and circularity that are higher in DH. Understanding the molecular processes underlying microglial sex differences and their potential implications for plasticity in specific brain regions is of major importance in physiological and pathological conditions.
Neuroimmune modulatory effects of the NLRP3 inflammasome: the role of sex and living environment in brain affecting conditions Miriam Ciani, Giovanna Rigillo, Beatrice Bertarini, Cristina Benatti, Silvia Alboni, Fabio Tascedda Frontiers in Immunology, 2025 The NLRP3 inflammasome is a master regulator of neuroinflammation, linking systemic perturbations to brain dysfunction and thereby influencing overall brain health. Its sensitivity to biological sex and environmental factors suggests that NLRP3 may act both as a contributor to sex-dependent disease mechanisms and a modifiable therapeutic target for pharmacological and non-pharmacological interventions. In this mini-review, we summarize emerging evidence on sex-specific differences in NLRP3 signaling that may contribute to disparities between males and females in disease incidence, symptomatology, and treatment response. Neuroinflammation-driven disorders, including atherosclerosis, neuropathic pain, substance use, and stress-related syndromes, show how sex influences NLRP3 inflammasome expression and activity with downstream effects on cognition and behavior. We also examine the modulatory influence of environmental factors, with emphasis on social behavior and environmental enrichment, as determinants of NLRP3 dynamics relevant to neurocognitive function and brain health. Overall, the findings suggest that NLRP3 acts as a central hub integrating sex and environmental influences, with broad implications for personalized interventions in brain-related disorders.
Stress, Hormones, and Metabolism Giulia Radighieri, Silvia Alboni Encyclopedia of Behavioral Neuroscience Volumes 1 3 Second Edition, 2021
Depressive Disorders Silvia Ferrari, Jordi Blanch, Shadi Lavasani, Steven C. Beall, Steven J. Gibson, Federica Maria Magarini, Silvia Alboni HIV Psychiatry A Practical Guide for Clinicians, 2021
Searching for New Possible Peripheral Biomarkers of Cognitive Decline in Down Syndrome: The Role of IL-18 Pathway and its Interaction with TGF-β1 and TNF-α M Grasso, A Fidilio, F L’Episcopo, M Recupero, C Barone, M Lovino, ... NeuroMolecular Medicine 28 (1), 12 , 2026 2026
Fatigue in Long COVID is associated with peripheral immunometabolic alterations affecting neuroimmune responses in the hippocampus. N Mariani, D Martins, M Kirkpatrick, N Tukiran, S Alboni, C Pariante, ... Translational psychiatry , 2026 2026
Cell line-specific modulation of inflammation by oestradiol in an in vitro model of antenatal depression M Kirkpatrick, S Alboni, F Imbeni, N Mariani, N Tukiran, E Mason-White, ... Brain, Behavior, and Immunity, 106212 , 2025 2025
Neuroimmune modulatory effects of the NLRP3 inflammasome: the role of sex and living environment in brain affecting conditions M Ciani, G Rigillo, B Bertarini, C Benatti, S Alboni, F Tascedda Frontiers in Immunology 16, 1711656 , 2025 2025 Citations: 1
The dietary ligands, omega-3 fatty acid endocannabinoids and short-chain fatty acids prevent cytokine-induced reduction of human hippocampal neurogenesis and alter the … G Mandal, S Alboni, N Cattane, M Marizzoni, S Saleri, N Arslanovski, ... Molecular Psychiatry 30 (11), 5338-5355 , 2025 2025 Citations: 8
Microbiota-gut-brain axis dysregulation in Alzheimer’s disease and its modulation through probiotic supplementation M Marizzoni, E Mombelli, S Alboni, M Rosa, DV Moretti, P Mirabelli, ... Brain, Behavior, and Immunity, 106138 , 2025 2025 Citations: 4
Para -Cresol and the Brain: Emerging Role in Neurodevelopmental and Neurodegenerative Disorders and Therapeutic Perspectives L Bertarini, F Imbeni, V Brighenti, I Martusciello, F Pellati, S Alboni ACS Pharmacology & Translational Science 8 (10), 3432-3452 , 2025 2025 Citations: 3
Interleukin 18 and the brain: neuronal functions, neuronal survival and psycho-neuro-immunology during stress S Alboni, F Tascedda, A Uezato, S Sugama, Z Chen, MCG Marcondes, ... Molecular Psychiatry 30 (7), 3197-3208 , 2025 2025 Citations: 10
Unraveling lipopolysaccharide-induced behavioral and molecular effects in Lymnaea stagnalis, an emerging model organism for translational neuroscience V Rivi, G Rigillo, S Alboni, JM Koene, L Pani, K Lukowiak, F Tascedda, ... International immunopharmacology 152, 114418 , 2025 2025 Citations: 4
Female mice exhibit similar long-term plasticity and microglial properties between the dorsal and ventral hippocampal poles E De Felice, BC Bobotis, G Rigillo, M Khakpour, EG de Andrade, ... Brain, behavior, and immunity 124, 192-204 , 2025 2025 Citations: 3
Time-and region-specific effect of vortioxetine on central LPS-induced transcriptional regulation of NLRP3 inflammasome M Ciani, G Rigillo, C Benatti, L Pani, JMC Blom, N Brunello, F Tascedda, ... Current neuropharmacology 23 (2), 196-208 , 2025 2025 Citations: 12
Targeted Metabolomics for the Analysis of p- Cresol in Mouse Brain: Impact of Biological Sex and Strain L Bertarini, F Imbeni, A Vilella, S Alboni, F Pellati ACS Chemical Neuroscience 16 (3), 452-461 , 2025 2025 Citations: 3
Exploring the frontiers of neuroinflammation: new horizons in research and treatment G Rigillo, S Alboni Current Issues in Molecular Biology 46 (10), 11665-11667 , 2024 2024 Citations: 3
Monocyte response to mitochondrial DAMPs in elderly subjects: a possible contribution to chronic inflammation and atherosclerosis G Zanini, G Sinigaglia, S Lopez Domenech, V Selleri, G Micheloni, ... European Heart Journal 45 (Supplement_1), ehae666. 3894 , 2024 2024
Ketamine prevents inflammation-induced reduction of human hippocampal neurogenesis via inhibiting the production of neurotoxic metabolites of the kynurenine pathway G Mandal, M Kirkpatrick, S Alboni, N Mariani, CM Pariante, A Borsini International Journal of Neuropsychopharmacology 27 (10), pyae041 , 2024 2024 Citations: 13
Behavioral and transcriptional effects of carnosine in the central ring ganglia of the pond snail Lymnaea stagnalis V Rivi, G Caruso, F Caraci, S Alboni, L Pani, F Tascedda, K Lukowiak, ... Journal of neuroscience research 102 (8), e25371 , 2024 2024 Citations: 12
Targeted metabolomics for the analysis of p-Cresol in mouse brain by HPLC-ESI-MS/MS: a new tool for drug discovery L Bertarini, F Imbeni, S Alboni, F Pellati Book of Abstracts_EFMC_ISMC , 2024 2024
Environmental quality modulates the endocannabinoid system along the gut-brain axis in a mouse model of LPS-induced neuroinflammation G Rigillo, C Benatti, Y Toscano, M Ciani, V Rivi, F Imbeni, L Pani, ... Science today for a better medicine tomorrow , 2024 2024
Microglial diversity along the hippocampal longitudinal axis impacts synaptic plasticity in adult male mice under homeostatic conditions. E De Felice, EG de Andrade, MT Golia, FG Ibanez, M Khakpour, ... GLIA 71, E490-E490 , 2023 2023
Indoleamine 2, 3-Dioxygenase 1 Mediates Survival Signals in chronic lymphocytic Leukemia via Kynurenine CG Atene, S Fiorcari, N Mesini, S Alboni, S Martinelli, M Maccaferri, ... The Immune Escape Mechanism and Novel Immunotherapeutic Strategies of … , 2023 2023 Citations: 1
MOST CITED SCHOLAR PUBLICATIONS
Interleukin 18 in the CNS S Alboni, D Cervia, S Sugama, B Conti Journal of neuroinflammation 7 (1), 9 , 2010 2010 Citations: 385
Shortened onset of action of antidepressants in major depression using acetylsalicylic acid augmentation: a pilot open-label study J Mendlewicz, P Kriwin, P Oswald, D Souery, S Alboni, N Brunello International clinical psychopharmacology 21 (4), 227-231 , 2006 2006 Citations: 311
Fractalkine receptor deficiency impairs microglial and neuronal responsiveness to chronic stress G Milior, C Lecours, L Samson, K Bisht, S Poggini, F Pagani, C Deflorio, ... Brain, behavior, and immunity 55, 114-125 , 2016 2016 Citations: 281
Fluoxetine effects on molecular, cellular and behavioral endophenotypes of depression are driven by the living environment S Alboni, RM Van Dijk, S Poggini, G Milior, M Perrotta, T Drenth, ... Molecular psychiatry 22 (4), 552-561 , 2017 2017 Citations: 266
Interplay between inflammation and neural plasticity: both immune activation and suppression impair LTP and BDNF expression MT Golia, S Poggini, S Alboni, S Garofalo, NC Albanese, A Viglione, ... Brain, behavior, and immunity 81, 484-494 , 2019 2019 Citations: 176
Sex-and age-specific differences in core body temperature of C57Bl/6 mice M Sanchez-Alavez, S Alboni, B Conti Age 33 (1), 89-99 , 2011 2011 Citations: 174
Rescue of IL-1β-induced reduction of human neurogenesis by omega-3 fatty acids and antidepressants A Borsini, S Alboni, MA Horowitz, LM Tojo, G Cannazza, KP Su, ... Brain, behavior, and immunity 65, 230-238 , 2017 2017 Citations: 153
Disease-induced neuroinflammation and depression C Benatti, J MC Blom, G Rigillo, S Alboni, F Zizzi, R Torta, N Brunello, ... CNS & Neurological Disorders-Drug Targets (Formerly Current Drug Targets-CNS … , 2016 2016 Citations: 140
Acetylsalicylic acid accelerates the antidepressant effect of fluoxetine in the chronic escape deficit model of depression N Brunello, S Alboni, G Capone, C Benatti, JMC Blom, F Tascedda, ... International clinical psychopharmacology 21 (4), 219-225 , 2006 2006 Citations: 136
Fluoxetine treatment affects the inflammatory response and microglial function according to the quality of the living environment S Alboni, S Poggini, S Garofalo, G Milior, H El Hajj, C Lecours, I Girard, ... Brain, behavior, and immunity 58, 261-271 , 2016 2016 Citations: 124
The transporters GlyT2 and VIAAT cooperate to determine the vesicular glycinergic phenotype KR Aubrey, FM Rossi, R Ruivo, S Alboni, GC Bellenchi, A Le Goff, ... Journal of Neuroscience 27 (23), 6273-6281 , 2007 2007 Citations: 120
Stress induces altered CRE/CREB pathway activity and BDNF expression in the hippocampus of glucocorticoid receptor-impaired mice S Alboni, F Tascedda, D Corsini, C Benatti, F Caggia, G Capone, ... Neuropharmacology 60 (7), 1337-1346 , 2011 2011 Citations: 117
Chronic treatment with the selective NOP receptor antagonist [Nphe1, Arg14, Lys15] N/OFQ-NH2 (UFP-101) reverses the behavioural and biochemical effects of unpredictable chronic … G Vitale, V Ruggieri, M Filaferro, C Frigeri, S Alboni, F Tascedda, ... Psychopharmacology 207 (2), 173-189 , 2009 2009 Citations: 93
Time-dependent effects of escitalopram on brain derived neurotrophic factor (BDNF) and neuroplasticity related targets in the central nervous system of rats S Alboni, C Benatti, G Capone, D Corsini, F Caggia, F Tascedda, ... European journal of pharmacology 643 (2), 180-187 , 2010 2010 Citations: 87
Interleukin 18 activates MAPKs and STAT3 but not NF-κB in hippocampal HT-22 cells S Alboni, C Montanari, C Benatti, M Sanchez-Alavez, G Rigillo, JMC Blom, ... Brain, behavior, and immunity 40, 85-94 , 2014 2014 Citations: 69
Chronic antidepressant treatments resulted in altered expression of genes involved in inflammation in the rat hypothalamus S Alboni, C Benatti, C Montanari, F Tascedda, N Brunello European journal of pharmacology 721 (1-3), 158-167 , 2013 2013 Citations: 69
Hypothalamic expression of inflammatory mediators in an animal model of binge eating S Alboni, MVM Di Bonaventura, C Benatti, ME Giusepponi, N Brunello, ... Behavioural brain research 320, 420-430 , 2017 2017 Citations: 68
Mapping of the full length and the truncated interleukin-18 receptor alpha in the mouse brain S Alboni, D Cervia, B Ross, C Montanari, AS Gonzalez, ... Journal of neuroimmunology 214 (1-2), 43-54 , 2009 2009 Citations: 58
What can we teach Lymnaea and what can Lymnaea teach us? V Rivi, C Benatti, K Lukowiak, C Colliva, S Alboni, F Tascedda, JMC Blom Biological Reviews 96 (4), 1590-1602 , 2021 2021 Citations: 56
Gut microbiota alterations promote traumatic stress susceptibility associated with p-cresol-induced dopaminergic dysfunctions S Laudani, SA Torrisi, S Alboni, TFS Bastiaanssen, C Benatti, V Rivi, ... Brain, Behavior, and Immunity 107, 385-396 , 2023 2023 Citations: 51