Erythropoietin attenuates Alzheimer-like memory impairments and pathological changes induced by amyloid β42 in mice

Li, Yi-pei; Yang, Guo-Jun; Jin, Li; Yang, Hongmei; Chen, Jie; Chai, Gaoshang; Wang, Li

doi:10.1016/j.brainres.2015.05.031

Cited by 36 publications

(24 citation statements)

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“…Moreover, it is proved to be neuroprotective in HD and stroke models AD and HD [114] Melatonin Improves the ultrastructure of mitochondria in the neurons of the CA1 region and prevents the decrease in the mitochondria-occupied portion of the neuronal volume in AD AD [115] Mori Fructus (ME) Decreases mitochondria depolarization, Cyt c release from mitochondria and caspase-3 activation induced by Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) toxicity in the mouse hippocampus AD [116] Erythropoietin (EPO) Alleviates the Aβ-induced mitochondrial dysfunction and apoptosis in brain AD [117] Linagliptin…”

Section: Methazolamide (Mtz)mentioning

confidence: 99%

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Jha

Kumar

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Mounting evidence suggests a link between metabolic syndrome (MetS) such as diabetes, obesity, non-alcoholic fatty liver disease in the progression of Alzheimer's disease (AD), Parkinson's disease (PD) and other neurodegenerative diseases (NDDs). For instance, accumulated Aβ oligomer is enhancing neuronal Ca release and neural NO where increased NO level in the brain through post translational modification is modulating the level of insulin production. It has been further confirmed that irrespective of origin; brain insulin resistance triggers a cascade of the neurodegeneration phenomenon which can be aggravated by free reactive oxygen species burden, ER stress, metabolic dysfunction, neuorinflammation, reduced cell survival and altered lipid metabolism. Moreover, several studies confirmed that MetS and diabetic sharing common mechanisms in the progression of AD and NDDs where mitochondrial dynamics playing a critical role. Any mutation in mitochondrial DNA, exposure of environmental toxin, high-calorie intake, homeostasis imbalance, glucolipotoxicity is causative factors for mitochondrial dysfunction. These cumulative pleiotropic burdens in mitochondria leads to insulin resistance, increased ROS production; enhanced stress-related enzymes that is directly linked MetS and diabetes in neurodegeneration. Since, the linkup mechanism between mitochondrial dysfunction and disease phenomenon of both MetS and NDDs is quite intriguing, therefore, it is pertinent for the researchers to identify and implement the therapeutic interventions for targeting MetS and NDDs. Herein, we elucidated the pertinent role of MetS induced mitochondrial dysfunction in neurons and their consequences in NDDs. Further, therapeutic potential of well-known biomolecules and chaperones to target altered mitochondria has been comprehensively documented. This article is part of a Special Issue entitled: Oxidative Stress and Mitochondrial Quality in Diabetes/Obesity and Critical Illness Spectrum of Diseases - edited by P. Hemachandra Reddy.

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Section: Methazolamide (Mtz)mentioning

confidence: 99%

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Jha

Kumar

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

View full text Add to dashboard Cite

show abstract

“…Specifically, relevant down-steam effects of these signalling cascades include activation of anti-apoptotic, antioxidant and anti-inflammatory signalling in neurons, glial and cerebrovascular endothelial cells, and promotion of dendritic sprouting, neurogenesis, hippocampal brain-derived neurotrophic factor (BDNF) and long-term potentiation 51 – 53 . Erythropoietin was also shown to exert neuroprotective effects by inhibiting the activity of the enzyme glycogen synthase kinase 3-beta (GSK3β) 54 , 55 , as will be discussed in greater detail later in this review. This may be particularly relevant in relation to mood disorders since GSK3β is a key activator of cell death and other functions involved in mood disorders, hippocampal volume, glucocorticoid regulation and neuroplasticity 56 – 58 .…”

Section: Epo Biologymentioning

confidence: 99%

GSK3β: a plausible mechanism of cognitive and hippocampal changes induced by erythropoietin treatment in mood disorders?

et al. 2018

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Mood disorders are associated with significant psychosocial and occupational disability. It is estimated that major depressive disorder (MDD) will become the second leading cause of disability worldwide by 2020. Existing pharmacological and psychological treatments are limited for targeting cognitive dysfunctions in mood disorders. However, growing evidence from human and animal studies has shown that treatment with erythropoietin (EPO) can improve cognitive function. A recent study involving EPO-treated patients with mood disorders showed that the neural basis for their cognitive improvements appeared to involve an increase in hippocampal volume. Molecular mechanisms underlying hippocampal changes have been proposed, including the activation of anti-apoptotic, antioxidant, pro-survival and anti-inflammatory signalling pathways. The aim of this review is to describe the potential importance of glycogen synthase kinase 3-beta (GSK3β) as a multi-potent molecular mechanism of EPO-induced hippocampal volume change in mood disorder patients. We first examine published associations between EPO administration, mood disorders, cognition and hippocampal volume. We then highlight evidence suggesting that GSK3β influences hippocampal volume in MDD patients, and how this could assist with targeting more precise treatments particularly for cognitive deficits in patients with mood disorders. We conclude by suggesting how this developing area of research can be further advanced, such as using pharmacogenetic studies of EPO treatment in patients with mood disorders.

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“…It is well-known that amyloid beta (Aβ) is a key molecule in AD and it is critical to develop a treatment that can arrest the Aβ-induced pathologic progression of AD. Li et al [38] study suggested that mice treated EPO (1000 U/kg) attenuated Aβ42-induced cognitive deficits and tau hyperphos-phorylation at multiple AD-related sites through the regulation of glycogen synthase kinase-3β and the Aβ42-induced mitochondrial dysfunction and apoptosis in brain. To the best of our knowledge, no literatures report about EPO treatment of AD patients.…”

Section: Introductionmentioning

confidence: 99%

Point of View about Erythropoietin in Treatment of Central Nervous System Diseases

Yang¹,

Li²,

Wu³

et al. 2017

J Alzheimers Dis Parkinsonism

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Erythropoietin attenuates Alzheimer-like memory impairments and pathological changes induced by amyloid β42 in mice

Cited by 36 publications

References 50 publications

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

GSK3β: a plausible mechanism of cognitive and hippocampal changes induced by erythropoietin treatment in mood disorders?

Point of View about Erythropoietin in Treatment of Central Nervous System Diseases

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