Alzheimer's disease, amyloid peptide and synaptic dysfunction

作者：Hemar Agnes; Mulle Christophe^*

来源：Medecine Sciences, 2011, 27(8-9): 733-736.

DOI：10.1051/medsci/2011278015

Alzheimer's disease, amyloid peptide and synaptic dysfunction
Alzheimer's disease (AD) is the first cause of dementia that leads to insidious and progressive loss of memory and cognitive functions. In the early stages of AD, there is a strong correlation between memory impairment and cortical levels of soluble amyloid-beta peptide oligomers (A beta). It has become clear that A beta disrupt glutamatergic synaptic function, which in turn may lead to the characteristic cognitive deficits. Conversely, experiments in rodents have conforted the notion that A beta omicron impairs synaptic transmission and plasticity, and that mouse models with increased production of these oligomers display cognitive impairment. Many studies have attempted to determine the mechanisms by which A beta omicron disrupt synaptic plasticity and mediate their detrimental effect, but the actual pathways are still poorly understood. Here we review this thriving area of research which aims at undertanding the mechanisms of synaptic dysfunction in the early phase of AD, and its consequences on the activity of neural circuits.

• 出版日期2011-9