Giuseppe Di Giovanni

TL;DR: It is concluded that answering key questions on the relationship between Aβ and tau pathology should lead to a better understanding of the nature of secondary tauopathies, especially AD, and open new therapeutic targets and strategies.

TL;DR: It is shown that extrasynaptic GABAA receptor–dependent 'tonic' inhibition is increased in thalamocortical neurons from diverse genetic and pharmacological models of absence seizures, identifying an apparently common cellular pathology in typical absence seizures that may have epileptogenic importance and highlight potential therapeutic targets for the treatment of absence epilepsy.

TL;DR: Data indicate that the central 5- HT system exerts a tonic and phasic inhibitory control on mesolimbic DA neuron activity and that 5-HT2C receptor subtypes are involved in this effect.

TL;DR: Evidence relating to the protective effects of aspirin or other NSAIDs on DAergic neurons in animal models of Parkinson's disease will be discussed and the pharmacological mechanisms by which these molecules can exert their neuroprotective effects will be reviewed.

TL;DR: Special emphasis is given to the serotonergic dorsal raphe nucleus (DRN) and noradrenergic LC, among the first to be affected by tau protein abnormalities in the course of sporadic AD, causing behavioral and cognitive symptoms of variable severity.