Accès ouvert
2025
article
OpenAlex
Michael G. Zaki, Mohamed Taha Moutaoufik, Mahboubeh Pordeli, Mohan Babu et autres
Glutamate receptors represent a potential target for neuroprotection in neurodegenerative neurological conditions. Perampanel, a non-competitive α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor (AMPAR) antagonist, is clinically approved for the management of epilepsy. Perampanel's neuroprotective effects have been reported in global and focal cerebral ischemia models, but …
ca
(code pays fourni par la source)
Accès ouvert
2025
preprint
OpenAlex
Michael G. Zaki, Mohamed Taha Moutaoufik, Mahboubeh Pordeli, Mohan Babu et autres
Glutamate receptors represent a potential target for neuroprotection in neurodegener-ative neurological conditions. Perampanel, a non-competitive α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor (AMPAR) antagonist, is clinically approved for the management of epilepsy. Perampanel’s neuroprotective ef-fects have been reported in global and focal cerebral ischemia models, but …
ca
(code pays fourni par la source)
Accès ouvert
2025
article
OpenAlex
Michael G. Zaki, Elisabet Jakova, Mahboubeh Pordeli, Elina Setork et autres
Stroke, the third leading cause of death worldwide, is a major cause of functional disability. Cerebral ischemia causes a rapid elevation of adenosine, the main neuromodulator in the brain. The inhibition of adenosine A2A receptors (A2ARs) has been introduced as a potential …
ca
(code pays fourni par la source)
Accès ouvert
2025
preprint
OpenAlex
Michael G. Zaki, Elisabet Jakova, Mahboubeh Pordeli, Elina Setork et autres
Stroke, the third leading cause of death worldwide, is a major cause of functional disability. Cerebral ischemia causes rapid elevation of adenosine, the main neuromodulator in the brain. Inhibition of adenosine A2A receptors (A2ARs) has been introduced as a potential target in …
ca
(code pays fourni par la source)
Accès ouvert
2021
article
OpenAlex
Qin Xin, Michael G. Zaki, Zhicheng Chen, Elisabet Jakova et autres
Chronic adenosine A1R stimulation in hypoxia leads to persistent hippocampal synaptic depression, while unopposed adenosine A2AR receptor stimulation during hypoxia/reperfusion triggers adenosine-induced post-hypoxia synaptic potentiation (APSP) and increased neuronal death. Still, the mechanisms responsible for this adenosine-mediated neuronal damage following hypoxia need …
ca, Égypte
(code pays fourni par la source)