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| 1 | Neuroprotective Effects of Dexmedetomidine in the Gerbil Hippocampus after Transient Global Ischemia显示文摘 | Johanna Kuhmonen Jaroslav Pokorny Riitta Miettinen Antti Haapalinna Jukka Jolkkonen Paavo Sr. Riekkinen Juhani Sivenius | 1997 | Anesthesiology1997，，2： | 2 |
| 2 | Effects of CXCR7-neutralizing antibody on neurogenesis in the hippocampal dentate gyrus and cognitive function in the chronic phase of cerebral ischemia显示文摘Stromal cell-derived factor-1 and its receptor CXCR4 are essential regulators of the neurogenesis that occurs in the adult hippocampal dentate gyrus.However,the effects of CXCR7,a new atypical receptor of stromal cell-derived factor-1,on hippocampal neurogenesis after a stroke remain largely unknown.Our study is the first to investigate the effect of a CXCR7-neutralizing antibody on neurogenesis in the dentate gyrus and the associated recovery of cognitive function of rats in the chronic stage of cerebral ischemia.The rats were randomly divided into sham,sham+anti-CXCR7,ischemia and ischemia+anti-CXCR7 groups.Endothelin-1 was injected in the ipsilateral motor cortex and striatum to induce focal cerebral ischemia.Sham group rats were injected with saline instead of endothelin-1 via intracranial injection.Both sham and ischemic rats were treated with intraventricular infusions of CXCR7-neutralizing antibodies for 6 days 1 week after surgery.Immunofluorescence staining with doublecortin,a marker for neuronal precursors,was performed to assess the neurogenesis in the dentate gyrus.We found that anti-CXCR7 antibody infusion enhanced the proliferation and dendritic development of doublecortin-labeled cells in the dentate gyrus in both ischemic and sham-operated rats.Spatial learning and memory functions were assessed by Morris water maze tests 30-32 days after ischemia.CXCR7-neutralizing antibody treatment significantly reduced the escape latency of the spatial navigation trial and increased the time spent in the target quadrant of spatial probe trial in animals that received ischemic insult,but not in sham operated rats.These results suggest that CXCR7-neutralizing antibody enhances the neurogenesis in the dentate gyrus and improves the cognitive function after cerebral ischemia in rats.All animal experimental protocols and procedures were approved by the Institutional Animal Care and Use Committee of China Medical University(CMU16089 R)on December 8,2016. | Bing-Chao Dong Mei-Xuan Li Xiao-Yin Wang Xi Cheng Yu Wang Ting Xiao Jukka Jolkkonen Chuan-Sheng Zhao Shan-Shan Zhao | 2020 | Neural Regeneration Research2020，15，6： | 2 |
| 3 | Time for a neurorestorative therapy in stroke显示文摘 | Pekka J? k? l? Jukka Jolkkonen | 2012 | Expert Opinion on Biological Therapy2012，，： | 1 |
| 4 | Preserving cognitive function in patients with Alzheimer's disease:The Alzheimer's disease neuroprotection research initiative(ADNRI)显示文摘The global trend toward aging populations has resulted in an increase in the occurrence of Alzheimer's disease(AD)and associated socioeconomic burdens.Abnormal metabolism of amyloid-β(Aβ)has been proposed as a significant pathomechanism in AD,supported by results of recent clinical trials using anti-Aβantibodies.Nonetheless,the cognitive benefits of the current treatments are limited.The etiology of AD is multifactorial,encompassing Aβand tau accumulation,neuroinflammation,demyelination,vascular dysfunction,and comorbidities,which collectively lead to widespread neurodegeneration in the brain and cognitive impairment.Hence,solely removing Aβfrom the brain may be insufficient to combat neurodegeneration and preserve cognition.To attain effective treatment for AD,it is necessary to(1)conduct extensive research on various mechanisms that cause neurodegeneration,including advances in neuroimaging techniques for earlier detection and a more precise characterization of molecular events at scales ranging from cellular to the full system level;(2)identify neuroprotective intervention targets against different neurodegeneration mechanisms;and(3)discover novel and optimal combinations of neuroprotective intervention strategies to maintain cognitive function in AD patients.The Alzheimer's Disease Neuroprotection Research Initiative's objective is to facilitate coordinated,multidisciplinary efforts to develop systemic neuroprotective strategies to combat AD.The aim is to achieve mitigation of the full spectrum of pathological processes underlying AD,with the goal of halting or even reversing cognitive decline. | Jie Liu Heleen van Beusekom Xian-Le Bu Gong Chen Paulo Henrique Rosado de Castro Xiaochun Chen Xiaowei Chen Andrew N.Clarkson Tracy D.Farr Yuhong Fu Jianping Jia Jukka Jolkkonen Woojin Scott Kim Paula Korhonen Shen Li Yajie Liang Guang-Hui Liu Guiyou Liu Yu-Hui Liu Tarja Malm Xiaobo Mao Joaquim Miguel Oliveira Mike M.Modo Pedro Ramos-Cabrer Karsten Ruscher Weihong Song Jun Wang Xuanyue Wang Yun Wang Haitao Wu Lize Xiong Yi Yang Keqiang Ye Jin-Tai Yu Xin-Fu Zhou Marietta Zille Colin L.Masters Piotr Walczak Boltze Johannes Xunming Ji Yan-Jiang Wang | 2023 | Neuroprotection2023，1，2： | 0 |
| 5 | The potential of a combined cell-based therapy and rehabilitation approach for stroke recovery显示文摘Activation of neuroprotective and particularly later neurorestorative mechanisms after stroke attempts to restore or compensate for lost functions.This potentially opens a wide window for restorative therapies to promote brain repair and improve long-term functional recovery.Although extensively demonstrated in the preclinical setting,the efficacy of cell-based therapies in stroke patients has been modest at best,if any at all.Translational failure may be due to the ineffective survival and integration of transplanted cells in pro-death stroke microenvironments that are not conducive for the structural reconstruction of damaged brain tissue and repair-related network reorganization.Optimal systemic delivery,timing,cell product,and dose remain open as well.Fortunately,a better understanding of the brain plasticity mechanisms underlying stroke recovery has ushered in a combination approach of cell-based therapy and rehabilitation that is aimed at achieving additive,synergistic,or even maximal beneficial effects.This novel combination therapy is not only targeted at promoting exogenous and endogenous cell survival and augmenting stand-alone restorative mechanisms but also at utilizing rehabilitation to facilitate a graft–host structural and functional integration and plasticity that would effectively remodel stroke tissue and restitute lost functions.This review presents an overview of the combination of cell-based therapy and experimental rehabilitation in stroke models.It also discusses associated shortcomings as well as proposes strategies to address them and help facilitate the advancement of this combination approach. | Abdulhameed Bakreen Jukka Jolkkonen | 2023 | Neuroprotection2023，1，2： | 0 |
| 6 | Join us on an amazing journey towards next-generation treatments for CNS disorders:Launch of Neuroprotection,a new high-quality journal in translational neuroscience显示文摘Translational medicine in neurodegenerative and neurovascular diseases is approaching a breakthrough point.Recent years have led to dramatic progress in both experimental and clinical research.Based on a much better and continuously increasing understanding of disease mechanisms,progression and pathophysiology,new therapies with an improved translational potential to protect tissue either against acute or chronic degeneration and even approaches potentially capable of repairing damaged brain tissue are emerging. | Xunming Ji Piotr Walczak Heleen M.M.van Beusekom Ana I.Casas Andrew Clarkson Tracy Farr Jukka Jolkkonen Yajie Liang Michel M.Modo Paulo H.Rosado-de-Castro Karsten Ruscher Yan-Jiang Wang Haitao Wu Marietta Zille Shen Li Johannes Boltze | 2023 | Neuroprotection2023，1，1： | 0 |
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