Neuroregeneration and dementia: new treatment options

Mitran, Smaranda Ioana; Cãtãlin, Bogdan; Sfredel, Veronica; Bălşeanu, Tudor-Adrian

doi:10.1186/2049-9256-1-12

Cited by 6 publications

(4 citation statements)

References 40 publications

(56 reference statements)

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“…BDNF and Ganglioside endogenous factors derived from the brain have prominent abilities in enhancing neurogenesis, but both of them show weak effects as exogenous treatments [10] . There are few drugs treating brain diseases by enhancing neurite outgrowth in the clinic [11] . In this study, based on an established in vitro neurite outgrowth model, we first discovered one natural product, 4,10-Aromadendranediol (ARDD), with the capability of promoting neurite outgrowth in neuronal cells.…”

Section: Introductionmentioning

confidence: 99%

The natural product 4,10-aromadendranediol induces neuritogenesis in neuronal cells in vitro through activation of the ERK pathway

Chang

Ruan

et al. 2016

Acta Pharmacol Sin

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Recent studies focus on promoting neurite outgrowth to remodel the central nervous network after brain injury. Currently, however, there are few drugs treating brain diseases in the clinic by enhancing neurite outgrowth. In this study, we established an NGF-induced PC12 differentiation model to screen novel compounds that have the potential to induce neuronal differentiation, and further characterized 4,10-Aromadendranediol (ARDD) isolated from the dried twigs of the Baccharis gaudichaudiana plant, which exhibited the capability of promoting neurite outgrowth in neuronal cells in vitro. ARDD (1, 10 μmol/L) significantly enhanced neurite outgrowth in NGF-treated PC12 cells and N1E115 cells in a time-dependent manner. In cultured primary cortical neurons, ARDD (5, 10 μmol/L) not only significantly increased neurite outgrowth but also increased the number of neurites on the soma and the number of bifurcations. Further analyses showed that ARDD (10 μmol/L) significantly increased the phosphorylation of ERK1/2 and the downstream GSK-3β, subsequently induced β-catenin expression and up-regulated the gene expression of the Wnt ligands Fzd1 and Wnt3a in neuronal cells. The neurite outgrowth-promoting effect of ARDD in neuronal cells was abolished by pretreatment with the specific ERK1/2 inhibitor PD98059, but was partially reversed by XAV939, an inhibitor of the Wnt/β-catenin pathway. ARDD also increased the expression of BDNF, CREB and GAP-43 in N1E115 cells, which was reversed by pretreatment with PD98059. In N1E115 cells subjected to oxygen and glucose deprivation (OGD), pretreatment with ARDD (1-10 μmol/L) significantly enhanced the phosphorylation of ERK1/2 and induced neurite outgrowth. These results demonstrated that the natural product ARDD exhibits neurite outgrowth-inducing activity in neurons via activation of the ERK signaling pathway, which may be beneficial to the treatment of brain diseases.

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Section: Introductionmentioning

confidence: 99%

The natural product 4,10-aromadendranediol induces neuritogenesis in neuronal cells in vitro through activation of the ERK pathway

Chang

Ruan

et al. 2016

Acta Pharmacol Sin

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“…Furthermore, stem‐cell transplantation appears to trigger neuroregeneration in the AD brain. The concept of neuroregeneration in the central nervous system (CNS) includes neurogenesis, neuroplasticity, and neurorestoration . Stem cells might enable new strategies for brain regeneration, because engrafted cells can activate endogenous neurogenesis to replace cells in the AD brain .…”

Section: General Issues Of Stem Cell Based Therapies For Admentioning

confidence: 99%

Stem‐Cell Challenges in the Treatment of Alzheimer's Disease: A Long Way from Bench to Bedside

Fan

Sun

Tang

et al. 2014

Medicinal Research Reviews

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Alzheimer's disease (AD) is the most prevalent type of dementia, and its neuropathology is characterized by deposition of insoluble β-amyloid peptides, intracellular neurofibrillary tangles, and the loss of diverse neurons. Current pharmacological treatments for AD relieve symptoms without affecting the major pathological characteristics of the disease. Therefore, it is essential to develop new and effective therapies. Stem-cell types include tissue-specific stem cells, such as neural stem cells and mesenchymal stem cells, embryonic stem cells derived from blastocysts, and induced pluripotent stem cells (iPSCs) reprogrammed from somatic cells. Recent preclinical evidence suggests that stem cells can be used to treat or model AD. The mechanisms of stem cell based therapies for AD include stem cell mediated neuroprotection and trophic actions, antiamyloidogenesis, beneficial immune modulation, and the replacement of the lost neurons. iPSCs have been recently used to model AD, investigate sporadic and familial AD pathogenesis, and screen for anti-AD drugs. Although considerable progress has been achieved, a series of challenges must be overcome before stem cell based cell therapies are used clinically for AD patients. This review highlights the recent experimental and preclinical progress of stem-cell therapies for AD, and discusses the translational challenges of their clinical application.

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“…En çok kemik iliği ve göbek kordonundan izole edilen mezenkimal kök hücreler kullanılmaktadır 70 . Alzheimer modeli oluşturulmuş hayvan deneylerinde kök hücre uygulamaları sonucu beyinde Aβ plaklarında azalma 71 , nöron rejenerasyonu ve nöronun yapısal fonksiyonlarındaki düzelmede artma 72 , azalan kolinerjik nöronlarda artma dolayısıyla asetilkolintransferaz aktivitesinde ve asetilkolin miktarında artma 73 görülmüştür. Ayrıca beyinde sinir büyüme faktörü ve beyin kaynaklı nörotrofik faktörün miktarında artış 74 , böylece nöron oluşumunda çoğalma tespit edilmiştir.…”

Section: Alzheimer Hastalığıunclassified

Nörodejeneratif Hastalıklarda Mezenkimal Kök Hücre Uygulamaları

Kıroğlu¹,

Aksu²

2015

Arşiv Kaynak Tarama Dergisi

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Neurodegenerative diseases are almost incurable, debilitating, and they might be fatal, because of limited neurogenesis in nervous system, presence of inhibitory substances and inhibition of recovery due to development of glial scar. Despite many treatment strategies of neurodegenerative diseases no full cure has been achieved. The successful results for mesenchymal stem cells applications on muscles, heart and liver diseases and the application of these cells to the damaged area in particular, hypoxia, inflammation and apoptosis promise hope of using them for neurodegenerative diseases. Mesenchymal stem cells applications constitute a vascular and neuronal phenotype in Parkinson's disease, Huntington's disease, Amyotrophic lateral sclerosis and Alzheimer's disease. Stem cells release bioactive agents that lead to suppression of local immune system, reduction of free radicals, increase in angiogenesis, inhibition of fibrosis, and apoptosis. In addition, tissue stem cells, increase neuronal healing, stimulate proliferation and differentiation. These findings show that stem cells might be a hope of a cure in the treatment of neurodegenerative diseases and intensive work on this issue should continue. Key words: Mesenchymal stem cells, therapy, neurodegenerative disease ÖZET Nörodejeneratif hastalıkların tedavisi oldukça güçtür ve bazen de öldürücüdür. Bunun nedeni santral sinir sisteminde nörogenesisin sınırlı olması, aktif inhibitör maddelerin bulunması ve glial skar dokusunun gelişmesi nedeniyle iyileşmenin engellenmesidir. Nörodejeneratif hastalıkların tedavisinde birçok uygulama yapılmasına rağmen tam bir kür elde etmek mümkün olmamıştır. Mezenkimal kök

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Neuroregeneration and dementia: new treatment options

Cited by 6 publications

References 40 publications

The natural product 4,10-aromadendranediol induces neuritogenesis in neuronal cells in vitro through activation of the ERK pathway

The natural product 4,10-aromadendranediol induces neuritogenesis in neuronal cells in vitro through activation of the ERK pathway

Stem‐Cell Challenges in the Treatment of Alzheimer's Disease: A Long Way from Bench to Bedside

Nörodejeneratif Hastalıklarda Mezenkimal Kök Hücre Uygulamaları

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