Alzheimerââ?¬â?¢s disease (AD) is a neurodegenerative disorder responsible for the majority of dementia cases in elderly people. It is\nwidely accepted that the main hallmarks of AD are not only senile plaques and neurofibrillary tangles but also reactive\nastrogliosis, which often precedes detrimental deposits and neuronal atrophy. Such phenomenon facilitates the regeneration of\nneural networks; however, under some circumstances, like in AD, reactive astrogliosis is detrimental, depriving neurons of the\nhomeostatic support, thus contributing to neuronal loss. We investigated the presence of reactive astrogliosis in 3Ã?â??Tg-AD mice\nand the effects of palmitoylethanolamide (PEA), a well-documented anti-inflammatory molecule, by in vitro and in vivo studies.\nIn vitro results revealed a basal reactive state in primary cortical 3Ã?â??Tg-AD-derived astrocytes and the ability of PEA to\ncounteract such phenomenon and improve viability of 3Ã?â??Tg-AD-derived neurons. In vivo observations, performed using\nultramicronized- (um-) PEA, a formulation endowed with best bioavailability, confirmed the efficacy of this compound.\nMoreover, the schedule of treatment, mimicking the clinic use (chronic daily administration), revealed its beneficial\npharmacological properties in dampening reactive astrogliosis and promoting the glial neurosupportive function. Collectively,\nour results encourage further investigation on PEA effects, suggesting it as an alternative or adjunct treatment approach for\ninnovative AD therapy.
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