RESUMO
Loss of synapses correlates well with cognitive decline in Alzheimer's disease (AD). However, the molecular mechanisms underlying the synaptic dysfunction and loss are not well understood. Synaptic vesicle (SV) recycling is a key process for synaptic transmission. A body of evidences suggested that malfunction or loss of the machinery for SV recycling occurred in AD, which could result in disruption of neuronal circuitry. In this article, we summarized the recent progress in the research of synaptic proteins for SV recycling and the pathological changes of some proteins in AD.
Assuntos
Doença de Alzheimer/fisiopatologia , Sinapses/fisiologia , Vesículas Sinápticas/fisiologia , Animais , Canais de Cálcio/fisiologia , Endocitose/fisiologia , Exocitose/fisiologia , Humanos , Vesículas Sinápticas/metabolismo , Sinaptofisina/fisiologia , Sinaptotagminas/fisiologiaRESUMO
OBJECTIVE: To observe the effects of Naoyikang (NYK) on expression of choline acetyltransferase (ChAT) in brain of rats with Alzheimer' s disease (AD). METHOD: Bilateral infusions of Ibotenic acid (IBO) into nucleus basalis of Meynert (NBM) using hamilton syringe and stereotaxic apparatus were adopted to establish the rat model of AD. After intragastrically administrated with different solution for 28 days, immunohistochemistry and Western-blot were adopted to study the expression of ChAT in frontal cortex of AD rats. RESULT: NYK could improve the morphology and increase the number of ChAT immunoreactive neurons, and significantly promote ChAT protein expression. CONCLUSION: NYK may be able to increase the synthesis of acetylcholine (ACh) through elevating the expression of ChAT protein, thus improving the level of brain ACh so as to protect central cholinergic neurons.
