Mitochondrial dysfunction, especially a defect in mitochondrial biogenesis, is 
an early and prominent feature of Alzheimer's disease (AD). Previous studies 
demonstrated that the number of mitochondria is significantly reduced in 
susceptible hippocampal neurons from AD patients. Neural stem cell (NSC) 
transplantation in AD-like mice can compensate for the neuronal loss resulting 
from amyloid-beta protein deposition. The effects of NSC transplantation on 
mitochondrial biogenesis and cognitive function in AD-like mice, however, are 
poorly understood. In this study, we injected NSCs or vehicle into 12-month-old 
amyloid precursor protein (APP)/PS1 transgenic mice, a mouse model of AD-like 
pathology. The effects of NSC transplantation on cognitive function, the amount 
of mitochondrial DNA, the expression of mitochondrial biogenesis factors and 
mitochondria-related proteins, and mitochondrial morphology were investigated. 
Our results show that in NSC-injected APP/PS1 (Tg-NSC) mice, the cognitive 
function, number of mitochondria, and expression of mitochondria-related 
proteins, specifically the mitochondrial fission factors (dynamin-related 
protein 1 [Drp1] and fission 1 [Fis1]) and the mitochondrial fusion factor optic 
atrophy 1 (OPA1), were significantly increased compared with those in 
age-matched vehicle-injected APP/PS1 (Tg-Veh) mice, whereas the expression of 
mitochondrial fusion factors mitofusion 1 (Mfn1) and Mfn2 was significantly 
decreased. These data indicate that NSC transplantation may enhance mitochondria 
biogenesis and further rescue cognitive deficits in AD-like mice.