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Diogo O. Souza

Researcher at Universidade Federal do Rio Grande do Sul

Publications -  561
Citations -  19653

Diogo O. Souza is an academic researcher from Universidade Federal do Rio Grande do Sul. The author has contributed to research in topics: Glutamate receptor & Excitotoxicity. The author has an hindex of 68, co-authored 534 publications receiving 17793 citations. Previous affiliations of Diogo O. Souza include Universidade Federal de Santa Catarina & Universidade Federal de Santa Maria.

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Caffeine and adenosine A(2a) receptor antagonists prevent beta-amyloid (25-35)-induced cognitive deficits in mice.

TL;DR: First direct in vivo evidence that caffeine and A(2A) receptor antagonists afford a protection against Abeta-induced amnesia, which prompts their interest for managing Alzheimer's disease is provided.
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Involvement of glutamate and reactive oxygen species in methylmercury neurotoxicity

TL;DR: This review addresses the mechanisms of methylmercury (MeHg)-induced neurotoxicity by examining the role of oxidative stress in mediating neuronal damage and provides a mechanistic overview on oxidative stress induced by MeHg that is triggered by a series of molecular events such as activation of various kinases, stress proteins and other immediate early genes culminating in cell damage.
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Quinolinic acid stimulates synaptosomal glutamate release and inhibits glutamate uptake into astrocytes.

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.
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Neuroprotection by caffeine and adenosine A2A receptor blockade of β-amyloid neurotoxicity

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.