review of PET in several diseases, including MS

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review of PET in several diseases, including MS

Postby frodo » Mon Jul 23, 2018 10:59 am

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Drugs evaluated in these studies include specific therapeutics which have already granted FDA licensure like interferon beta, [50] glatiramer acetate, [51] and fingolimod [52, 53] in MS, nonspecific drugs which exert anti-inflammatory effects, [54, 55] and new therapeutical class-targeting biochemical pathways involved in neurodegenerative disorder such as the hydrolysis of neuroprotective endocannabinoid [56] and oxidative stress [57].

Microglial activation plays a central role in maintaining the central chronic inflammation in MS [58]. MS is a chronic autoimmune disease of the CNS where the migration of myelin-reactive T-cells into the CNS is followed by microglial activation, recruitment of peripheral macrophages, and oligodendrocytes destruction [59]. Fingolimod blocks the egress of lymphocytes from secondary lymphoid tissues and thereby prevents their entry into the CNS [60]. In line with its mechanism of action, PET imaging showed that fingolimod reduced microglial activation [52, 53], especially in T2 lesion area [53]. Glatiramer acetate, a synthetic polypeptide resembling myelin basic protein, acts further downstream deceiving immune system and inducing immunomodulatory Th2 cells [61]. Ratchford et al. [51] provided proof of concept that microglia PET imaging with 11C-PK11195 could also be a tool to assess disease-modifying drugs for relapsing-remitting multiple sclerosis (RRMS) efficacity. Indeed, radiopharmaceutical binding potential per unit volume was statistically decreased in the whole brain after one year of glatiramer acetate. This result supported the in vitro evidence of its mechanism of action in which an inhibition of transformation to an activated microglia form could be responsible for therapeutic effects
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