Downregulation of brain-derived neurotrophic factor (BDNF) in the hippocampus occurs early in the progression of Alzheimer’s disease (AD). Since BDNF plays a critical role in neuronal survival and dendrite growth, BDNF upregulation may contribute to rescue dendrite atrophy and cell loss in AD. Low-level laser therapy (LLLT) has been demonstrated to regulate neuronal function both in vitro and in vivo. In the present study, we found that LLLT rescued neurons loss and dendritic atrophy via the increase of both BDNF mRNA and protein expression. In addition, dendrite growth was improved after LLLT, characterized by upregulation of PSD95 expression, and the increase in length, branching, and spine density of dendrites in hippocampal neurons. Together, these studies suggest that upregulation of BDNF with LLLT can ameliorate Aβ-induced neurons loss and dendritic atrophy, thus identifying a novel pathway by which LLLT protects against Aβ-induced neurotoxicity. Our research may provide a feasible therapeutic approach to control the progression of Alzheimer’s disease.
Cardiolipin is a unique and ubiquitous diphosphatidylglycerol phospholipid, located exclusively in inner
membrane of mitochondria and particularly intermembrane contact sites. Cardiolipin is essential for
mitochondrial to maintain its functions. Numerous mitochondrial proteins and processes require the presence of
cardiolipin. Recent researches gradually confirm that cardiolipin participates in several mitochondria-dependent
apoptotic steps: interactions between cardiolipin and cytochrome c, Bid and caspase-8 have now been
established. These functions are associated with the redistribution of cardiolipin in mitochondria. However, the
exact mechanism of the redistribution, which happens at the early stage of apoptosis, is still controversial. In this
study, we used 10-N-nonyl-3, 6-bis (dimethylamino) acridine (10-N-nonyl acridine orange), a specific probe for
cardiolipin to monitor changes of cardiolipin redistribution during apoptosis. We demonstrated that during
apoptosis cardiolipin moves to the outer leaflet of mitochondrial inner membrane from the inner leaflet, where it
used to be riched in. We also found that ROS (reactive oxygen species) may have association with the
redistribution of cardiolipin.
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