RvE1 treatment prevents memory loss and neuroinflammation in the Ts65Dn mouse model of Down syndrome

Hamlett, Eric D.; Hjorth, Erik; Ledreux, Aurélie; Gilmore, Anah; Schultzberg, Marianne; Granholm, Ann Charlotte

doi:10.1002/glia.23779

Cited by 27 publications

(24 citation statements)

References 54 publications

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“…RvE1 is a trihydroxy derivative of the polyunsaturated fatty acid EPA, and is found in sh oil and sea food. RvE1 possesses a remarkable treatment effect for many in ammation-related diseases and conditions when administered via subcutaneous injection, intraperitoneal injection, intraplantar injection and intrathecal injection [11,[13][14][15][16][17]25]. In this study, after RvE1 was administered via intraperitoneal injection, we observed amelioration of inner ear damage after irradiation and changes of some of the in ammatory factors associated the in ammatory response.…”

Section: Discussionsupporting

confidence: 50%

A unique radioprotective effect of resolvin E1 reduces irradiation-induced damage to the inner ear by inhibiting the inflammatory response

Zhang

Niu

et al. 2020

Preprint

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Background: In addition to the direct effects of irradiation, the induced inflammatory response may play an important role in the damage to the inner ear caused by radiotherapy for the treatment of head and neck cancers. Resolvin E1 (RvE1) has anti-inflammatory activity, acting by reducing neutrophil infiltration and proinflammatory cytokine expression. Therefore, in this study we sought to confirm whether the inflammation induced by irradiation was involved in damage to the inner ear after radiotherapy and to investigate the protective effect and underlying mechanism of RvE1 using mouse models. Methods: A dose of RvE1 was delivered by intraperitoneal injection to mice before irradiation. Changes in the auditory brainstem response (ABR), relative balance ability, inner ear morphology and the expression levels of inflammatory factors in the inner ear were analyzed on days 7 and 14 after irradiation and compared among different experimental groups. Results: Changes of ABR and relative balance ability showed the inner functions of experimental mice presented severe damage after irradiation, but the damage was significantly alleviated after RvE1 pretreatment compared to irradiation alone. Morphological analysis of the inner ear showed severe damage to the cochlea and vestibule after irradiation. In contrast, damage to the cochlea and vestibule was significantly reduced in the RvE1-pretreated group compared to that in the irradiation alone group. Along with these functional and morphological changes, the mRNA expression level of anti-inflammatory factors interleukin-2 was significantly increased, while those of proinflammatory factors interleukin-6 and tumor necrosis factor-α were significantly decreased in the inner ear of mice after RvE1 pretreatment compared to irradiation alone. Conclusions: We believe that inflammation induced by irradiation is involved in the damage to the inner ear caused by radiotherapy, and that RvE1 reduces the damage caused by irradiation to the inner ear by regulating the induced inflammatory response.

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Section: Discussionsupporting

confidence: 50%

A unique radioprotective effect of resolvin E1 reduces irradiation-induced damage to the inner ear by inhibiting the inflammatory response

Zhang

Niu

et al. 2020

Preprint

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“…Dysfunctional resolution of chronic neuroinflammation is now considered as a driver of AD pathogenesis. Resolution of neuroinflammation by pro-homeostatic lipids (called specialized pro-resolving mediators, SPMs) might be a rational treatment in early stages of AD [231].…”

Section: Discussionmentioning

confidence: 99%

Oligomerization and Conformational Change Turn Monomeric β-Amyloid and Tau Proteins Toxic: Their Role in Alzheimer’s Pathogenesis

2020

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The structural polymorphism and the physiological and pathophysiological roles of two important proteins, β-amyloid (Aβ) and tau, that play a key role in Alzheimer’s disease (AD) are reviewed. Recent results demonstrate that monomeric Aβ has important physiological functions. Toxic oligomeric Aβ assemblies (AβOs) may play a decisive role in AD pathogenesis. The polymorph fibrillar Aβ (fAβ) form has a very ordered cross-β structure and is assumed to be non-toxic. Tau monomers also have several important physiological actions; however, their oligomerization leads to toxic oligomers (TauOs). Further polymerization results in probably non-toxic fibrillar structures, among others neurofibrillary tangles (NFTs). Their structure was determined by cryo-electron microscopy at atomic level. Both AβOs and TauOs may initiate neurodegenerative processes, and their interactions and crosstalk determine the pathophysiological changes in AD. TauOs (perhaps also AβO) have prionoid character, and they may be responsible for cell-to-cell spreading of the disease. Both extra- and intracellular AβOs and TauOs (and not the previously hypothesized amyloid plaques and NFTs) may represent the novel targets of AD drug research.

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“…Grafted hESC-MGE progenitor cells differentiated into active GABAergic neurons with mature firing patterns, showing their integration into the host hippocampal circuitry and suggesting a synaptic mode of action [ 34 , 35 ]. Alternatively, hESC-interneuron grafts can ameliorate memory impairment through release of GABA or neurotrophic factors that protect hippocampal neurons and synaptic integrity, or by releasing factors that reduce inflammation which is known to impair learning and memory [ 62 , 63 ].…”

Section: Main Textmentioning

confidence: 99%

Human Pluripotent Stem Cells-Based Therapies for Neurodegenerative Diseases: Current Status and Challenges

Ford

Pearlman

Ruan

et al. 2020

Cells

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Neurodegenerative diseases are characterized by irreversible cell damage, loss of neuronal cells and limited regeneration potential of the adult nervous system. Pluripotent stem cells are capable of differentiating into the multitude of cell types that compose the central and peripheral nervous systems and so have become the major focus of cell replacement therapies for the treatment of neurological disorders. Human embryonic stem cell (hESC) and human induced pluripotent stem cell (hiPSC)-derived cells have both been extensively studied as cell therapies in a wide range of neurodegenerative disease models in rodents and non-human primates, including Parkinson’s disease, stroke, epilepsy, spinal cord injury, Alzheimer’s disease, multiple sclerosis and pain. In this review, we discuss the latest progress made with stem cell therapies targeting these pathologies. We also evaluate the challenges in clinical application of human pluripotent stem cell (hPSC)-based therapies including risk of oncogenesis and tumor formation, immune rejection and difficulty in regeneration of the heterogeneous cell types composing the central nervous system.

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RvE1 treatment prevents memory loss and neuroinflammation in the Ts65Dn mouse model of Down syndrome

Cited by 27 publications

References 54 publications

A unique radioprotective effect of resolvin E1 reduces irradiation-induced damage to the inner ear by inhibiting the inflammatory response

A unique radioprotective effect of resolvin E1 reduces irradiation-induced damage to the inner ear by inhibiting the inflammatory response

Oligomerization and Conformational Change Turn Monomeric β-Amyloid and Tau Proteins Toxic: Their Role in Alzheimer’s Pathogenesis

Human Pluripotent Stem Cells-Based Therapies for Neurodegenerative Diseases: Current Status and Challenges

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