Autor(es):
Ribeiro, Joaquim A. 
; Sebastião, Ana M.
Data: 2010
Identificador Persistente: http://hdl.handle.net/10451/6361
Origem: Repositório da Universidade de Lisboa
Assunto(s): Adenosine; Alzheimer’s disease; Huntington’s disease; Parkinson’s disease; Schizophrenia; Cognition
Descrição
© 2010 – IOS Press and the authors. All rights reserved Caffeine causes most of its biological effects via antagonizing all types of adenosine receptors (ARs): A1, A2A, A3,
and A2B and, as does adenosine, exerts effects on neurons and glial cells of all brain areas. In consequence, caffeine, when
acting as an AR antagonist, is doing the opposite of activation of adenosine receptors due to removal of endogenous adenosinergic tonus. Besides AR antagonism, xanthines, including caffeine, have other biological actions: they inhibit phosphodiesterases (PDEs) (e.g., PDE1, PDE4, PDE5), promote calcium release from intracellular stores, and interfere with GABA-A receptors.
Caffeine, through antagonism of ARs, affects brain functions such as sleep, cognition, learning, and memory, and modifies brain
dysfunctions and diseases: Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, Epilepsy, Pain/Migraine, Depression,
Schizophrenia. In conclusion, targeting approaches that involve ARs will enhance the possibilities to correct brain dysfunctions,
via the universally consumed substance that is caffeine.
