Abstract
AbstractBackgroundAlzheimer's disease (AD) is characterized by the accumulations of amyloid beta and neurofibrillary tangles in brain tissue; however, AD is multifactorial and different etiopathogenic mechanisms involves that can affect mitochondrial function that are associated with AD. In the current study, we investigated the effect of lithium on mitochondrial function in AD.MethodNeuronal cells were isolated separately from hippocampal of brain tissue of control mice (C57BL/6) and 3xTg model of AD. Mitochondrial oxygen consumption rate (OCR), mitochondrial Cytochrome C Oxidase (COX) activity, and total ATP activity were measured in control vs. AD neurons after one day and seven days dose‐dependent treatment with lithium.ResultIn the present study, short and long term lithium treatment significantly increased (p<0.05) mitochondrial OCR, COX, and total ATP level in 3xTg neurons. However, lithium had no effect on energy metabolism in control neurons. Together, these data indicate that lithium improves mitochondrial function under pathological states.ConclusionOverall, these results have important implications for the treatment of disorders in which brain energy regulation are compromised, including AD. Particularly, our results highlight a role for lithium in regulating bioenergetics in early stage AD and suggest that neuronal cells may be a crucial therapeutic target for preventing AD.
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