Acta Neuropharmacologica››2011,Vol. 1››Issue (1): 1-15.

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Neuron-synapse loss and dementias

ZHANG Juntian

    • Online:2011-02-26Published:2011-10-20

    Abstract:Basic and clinical study of Alzheimer’s disease showed that senile plagues and neurofibrillary tangle are not related to the degree of cognitive impairment. Synaptic loss occur in Alzheimer’s disease and other neurodegenerative dementias which block LTP,induce neuropsychological dysfunction and memory deficit . Neuron-synapses or synaptic loss was considered as main cause of dementias. Several hidden toxins such as oligomer of Aβ and phosphorylated Tau,glutamate receptor at extrasynaptic region and shank protein can lead to synaptic loss. Therefore,strategy for AD treatment is that ① To clean oligomer by native oligomer of Aβ immunotherapy. ②To maintain the normal homeostasis of synaptic protein by mTOR(a protein kinase) and UPS. ③To activate synaptic NMDA receptors or block extrasynaptic NMDA receptors. ④To increase hippocampal neurogenesis and synaptogenesis. In our recent study,ginsenoside Rg1 and Ppt were proved to increase synaptic plasticity in both efficacy and structure as well as increase neurogenesis bothin vitroandin vivounder physiological and pathological circumstances,indicating that they are promising agents for preventing and treatment of dementias and many kinds of memory impairment.

    Key words:neuron-synapse loss,dementias,cognition,long-term ,potentiation(LTP),NMDA receptor,gensenoside Rg1 and Ppt,neurogenesis,synaptogenesis

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