Amyloid β 1-42 induces hypometabolism in human stem cell-derived neuron and astrocyte networks.

ABSTRACT: Alzheimer's disease (AD) is the most common form of dementia, affecting more than 35 million people worldwide. Brain hypometabolism is a major feature of AD, appearing decades before cognitive decline and pathologic lesions. To date, the majority of studies on hypometabolism in AD have used transgenic animal models or imaging studies of the human brain. As it is almost impossible to validate these findings using human tissue, alternative models are required. In this study, we show that human stem cell-derived neuron and astrocyte cultures treated with oligomers of amyloid beta 1-42 (Aβ1-42) also display a clear hypometabolism, particularly with regard to utilization of substrates such as glucose, pyruvate, lactate, and glutamate. In addition, a significant increase in the glycogen content

SUBMITTER: Tarczyluk MA 

PROVIDER: S-EPMC4528011 | biostudies-literature | 2015 Aug

REPOSITORIES: biostudies-literature