Experimental Neuro Psychobiology Laboratory

Rome, Italy

Experimental Neuro Psychobiology Laboratory

Rome, Italy
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Bossu P.,Experimental Neuro psychobiology Laboratory | Ciaramella A.,Experimental Neuro psychobiology Laboratory | Salani F.,Experimental Neuro psychobiology Laboratory | Vanni D.,Experimental Neuro psychobiology Laboratory | And 3 more authors.
Current Pharmaceutical Design | Year: 2010

A large body of evidence on brain development and ageing has revealed that inflammatory processes profoundly affect brain functions during life span of mammalians, including humans. Activation of innate immune mechanisms leading to pro-inflammatory cytokine up-regulation is involved in devastating and disabling human brain illnesses, as Alzheimer's disease (AD), a progressive neurodegenerative disease that causes dementia in the elderly. Emerging data indicate that the cytokine Interleukin (IL)-18, one of the key mediator of inflammation and immune response, has relevance in the physiopathological processes of the brain, by ultimately influencing the integrity of neurons and putatively contributing to AD. In this review, the relationship between specific IL-18-mediated processes and AD neurodegeneration is summarized and clinical studies pointing to a role of the cytokine in the pathology are discussed. Altogether, the presented data indicate that a more complete knowledge of the molecular mechanisms underlying IL-18 implication in neuroinflammatory and neurodegenerative pathways could contribute toward the development of new therapeutic strategies for AD. © 2010 Bentham Science Publishers Ltd.


Ciaramella A.,Experimental Neuro Psychobiology Laboratory | Della Vedova C.,Post Coma Unit | Salani F.,Experimental Neuro Psychobiology Laboratory | Viganotti M.,Experimental Neuro Psychobiology Laboratory | And 5 more authors.
NeuroImmunoModulation | Year: 2013

Objective: A long-lasting neuroinflammatory cascade may lead to the progression of brain damage, favoring neurodegeneration and cognitive impairment in patients with traumatic brain injury (TBI), but the potential mechanisms underlying this sequence of events remain elusive. Here we aimed to evaluate the impact of interleukin (IL)-18, a proinflammatory cytokine elevated in post-acute head injury and associated with neurodegeneration, on the long-term outcome of patients with chronic TBI. Methods: The serum content of IL-18 was evaluated in 16 patients with severe TBI, during their rehabilitation phase, and in a matched group of 16 healthy controls. The disability of the enrolled patients was evaluated by means of the Glasgow Outcome Scale, Levels of Cognitive Functioning, and the Disability Rating Scale. Results: The circulating levels of IL-18 were significantly increased in chronic TBI patients, as compared to healthy subjects, and correlated with the patients' cognitive impairment and disability severity. Conclusions: IL-18 may contribute to the long-term outcome and neurodegeneration in TBI patients. Even though further studies are needed to understand the molecular mechanisms underlying the effects of IL-18 on TBI progression and its associated drop in cognitive function, a possible role of this cytokine as a therapeutic target in TBI can be envisaged. © 2013 S. Karger AG, Basel.

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