Neuroprotection induced by NMDA preconditioning as a strategy to understand brain tolerance mechanism

Excitotoxicity refers to toxicity caused by abnormal concentrations of glutamate in the synaptic cleft that may lead to neuronal death. Since its description, the phenomenon of glutamatergic excitotoxicity has been implicated in the physiopathology of a wide range of neurological and psychiatric disorders, from acute brain damage such as traumatic brain injury, ischemia as well as chronic condi- tions like epilepsy, depression and neurodegenerative pathologies such as Huntington＇s, Parkinson＇s and Alzheimer＇s diseases. Exces- sive stimulation of glutamatergic receptors, mainly N-methyl-D-as- partate （NMDA） receptors （NMDAR）, can have numerous adverse effects on the cell viability, including increased nitric oxide release （NO）, activation of proteases, increased production of reactive oxygen （ROS） and nitrogen （RNS） species and massive influx of calcium ions （Ca2＋）, resulting in cell death. Thus, the use of strategies that modulate the excitotoxic cell damage represents a perspective for the treatment of diseases such as Parkinson＇s and Alzheimer＇s diseases, ischemia, traumatic brain injury （TBI） and seizures.

Targeting the guanine-based purinergic system in Alzheimer's disease

Alzheimer’s disease（AD）is the main cause of dementia worldwide and affects approximately 5%of people with 65 years or older.The estimated increase in the elderly population suggests that cases of AD will rise in the next years.