Modeling and Therapeutic Strategies of Pluripotent Stem Cells for Alzheimer’s Disease

Abstract

Copyright: © 2013 Gu H. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases, which is characterized by a progressive and age-related chronic loss of neurons in extensive brain areas, such as cerebral cortex and hippocampus, one of the most prominent being the basal forebrain cholinergic neurons (BFCN). In clinic, patients suffer from impairment of memory and cognitive function, language breakdown and eventually long-term memory loss. The burden of AD is heavy to patient’s families and the whole society. The pathological findings of AD are senile plaques, neurofibrillary tangles and neuronal cell death. Senile plaques and neurofibrillary tangles are mainly consisted of β-amyloid (Aβ) peptides, which are formed by the cleavage of amyloid precursor protein (APP) by βand γ-secretase. In the end, accumulation of Aβ peptides in neurons causes neuronal degeneration and cell death [1,2]. Although previous studies already showed the effects of Aβ peptides on cultured mammal neurons, how Aβ peptides affect human neurons, especially neurons from AD patients, are still not understood. On the other hand, although neurotrophic factors application, such as nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), have showed functional recovery in animal model of AD and several drugs for the treatment of AD has been approved by FDA and have shown the improvement of cognitive function and memory of AD patient, it is still challenge to delay and reverse the neuronal degeneration and cell death [3-5].