Lisiane O. Porciúncula

TL;DR: A2ARs play a crucial role in the development of Aβ-induced synaptotoxicity leading to memory dysfunction through a p38 MAPK (mitogen-activated protein kinase)-dependent pathway and provide a molecular basis for the benefits of caffeine consumption in AD.

TL;DR: Investigating the effects of QA on the glutamatergic system from rat brain, it is demonstrated that QA (from 0.1 to 10mM) had no effect on synaptosomal L-[3H]glutamate uptake, and data provide additional evidence that neurotoxicity ofQA may be also related to disturbances on the glutamate transport system, which could result in the neurological manifestations observed when this organic acid accumulates in the brain.

TL;DR: First in vitro evidence to suggest that adenosine A2A receptors may be the molecular target responsible for the observed beneficial effects of caffeine consumption in the development of Alzheimer's disease is observed.

TL;DR: It is shown that caffeine prevents the maladaptive changes caused by CUS in a manner mimicked by the selective blockade of adenosine A2A receptors (A2AR), suggesting A2AR as candidate targets to alleviate the consequences of chronic stress on brain function.

TL;DR: Caffeine consumption prevented the STZ-induced memory impairment and neurodegeneration as well as the upregulation of A2AR, providing the first demonstration that caffeine prevents sporadic dementia and implicate the control of central A2 AR as its likely mechanism of action.