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Aims DJ-1 is a key redox-reactive neuroprotective protein implicated in regulation of oxidative stress after stroke. However, the molecular mechanism, especially the role of mitochondrial function, by which DJ-1 protects neural cells in stroke remains to be elucidated. The aim of this study was to reveal whether DJ-1 translocates into the mitochondria in exerting neuroprotection against oxidative stress. In particular, we examined DJ-1 secretion from primary rat neural cells (PRNCs) exposed to experimental stroke. Methods PRNCs were exposed to the oxygen glucose deprivation (OGD), an established in vitro stroke model, and DJ-1 translocation was measured by immunocytochemistry and its secretion detected by ELISA. Results Under OGD, DJ-1 translocated into the healthy mitochondria, and significant levels of DJ-1 protein were detected. Treatment with anti-DJ-1 antibody reduced cell viability and mitochondrial activity, and increased glutathione level. Interestingly, OGD reversed the ratio of astrocyte/ neuron cells (6/4 to 4/6). Conclusion Altogether, these results revealed that DJ-1 participates in the acute endogenous neuroprotection after stroke via the mitochondrial pathway. That DJ-1 was detected immediately after stroke and efficiently translocated into the mitochondria offer a new venue for developing neuroprotective and/ or neurorestorative strategies against ischemic stroke.

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BackgroundThis study aims to create a convenient reference for both clinicians and researchers so that vis-à-vis comparisons between brain disorders can be made quickly and accurately. We report here the incidence and prevalence of the major adult-onset brain disorders in the United States using a meta-analysis approach.Material and MethodsEpidemiological figures were collected from the most recent, reliable data available in the research literature. Population statistics were based on the most recent census from the US Census Bureau. Extrapolations were made only when necessary. The most current epidemiological studies for each disorder were chosen. All effort was made to use studies based on national cohorts. Studies reviewed were conducted between 1950 and 2009. The data of the leading studies for several neurological studies was compiled in order to obtain the most accurate extrapolations. Results were compared to commonly accepted values in order to evaluate validity.ResultsIt was found that 6.75% of the American adult population is afflicted with brain disorders. This number was eclipsed by the 8.02% of Floridians with brain disorders, which is due to the large aged population residing in the state.ConclusionsThere was a noticeable lack of epidemiological data concerning adult-onset brain disorders. Since approximately 1 out of every 7 households is affected by brain disorders, increased research into this arena is warranted.

DJ-1 is an important redox-reactive neuroprotective protein implicated in regulation of oxidative stress after ischemia. However the molecular mechanism, especially the mitochondrial function, by which DJ-1 protects neuronal cells in stroke remains to be elucidated. The aim of this study was to reveal whether DJ-1 translocates into the mitochondria in exerting neuroprotection against an in vitro model of stroke. Human neural progenitor cells (hNPCs) were initially exposed to oxygen–glucose deprivation and reperfusion injury, and thereafter, DJ-1 translocation was measured by immunocytochemistry and its secretion by hNPCs was detected by enzyme-linked immunosorbant assay (ELISA). Exposure of hNPCs to experimental stroke injury resulted in DJ-1 translocation into the mitochondria. Moreover, significant levels of DJ-1 protein were secreted by the injured hNPCs. Our findings revealed that DJ-1 principally participates in the early phase of stroke involving the mitochondrial pathway. DJ-1 was detected immediately after stroke and efficiently translocated into the mitochondria offering a new venue for developing treatment strategies against ischemic stroke.