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Volume 5, Issue 5 (Suppl) J Neurol Disord, an open access journal
ISSN: 2329-6895 CNS 2017
October 02-03, 2017
Page 19
Notes:
conferenceseries.com
3rd International Conference on
Central Nervous System Disorders and Therapeutics
October 02-03, 2017 Vienna, Austria
Antonio Scilimati, J Neurol Disord 2017, 5:5(Suppl)
DOI: 10.4172/2329-6895-C1-022
Neuroinflammation: Prodrome of neurological and neurodegenerative diseases
Brain inflammatory response, termed neuroinflammation, is crucial to protect the CNS. However, uncontrolled or
prolonged neuroinflammation is harmful and could induce neuronal damage. This is particularly relevant in neurological
and neurodegenerative diseases (i.e., Alzheimer and Parkinson diseases, amyotrophic lateral sclerosis, multiple sclerosis,
traumatic brain injury, HIV dementia, and prion diseases), which are typified by evidence of microglial activation and
neuroinflammation. Microglia, the resident immune cells in the brain, plays a role in immune surveillance. Once exposed to
immunological challenges such as invading pathogens and neuronal injuries, microglia readily activate and undergo changes
in morphology (hypertrophy), number (proliferation), and function (phagocytosis). As a consequence of their activation,
microglia produce many pro-inflammatory factors and neurotoxic mediators including complement, arachidonic acid and its
lipid metabolites (prostaglandins), cytokines, chemokines, nitric oxide and free radicals, several of which contribute directly to
neuronal injury. Among the mechanisms involved into the neuroinflammatory complex network, the cyclooxygenase-1 (COX-
1) (predominantly localized in microglia) plays a previously unrecognized role in the neuroinflammation as demonstrated by
the attenuation of the inflammatory response and neuronal loss due to the genetic ablation or pharmacological inhibition of
COX-1 activity. COX-2, the other known COX isoform, mainly localized in pyramidal neurons, is expected to predominantly
contribute to increase prostaglandin biosynthesis in response to insults that directly challenge neurons, such as ischemia and
excitotoxicity. In this context, the action of highly selective COX-1 inhibitors compared to coxibs (selective COX-2 inhibitors)
in in vitro and in vivo neuroinflammatory state will be presented.
Biography
Antonio Scilimati graduated cum laude in Chemistry at the University of Bari (Italy) and PhD at the University of Wisconsin (USA). He worked for 4 years at MerckSerono
plant producing recombinant drugs. Now, he is an Associate Professor at University of Bari, teaching Medicinal Chemistry. In "Medicinal Science", he uses the theranostic
approach to target the cyclooxygenase (COX)-1 as a novel biomarker in oncology and neuroinflammation.
Antonio Scilimati
University of Bari, Italy