eBooks Press Release — NEWS | The Seventh Volume of Topics in Anti-Cancer Research Is Now Available

 

 

Topics in Anti-Cancer Research (Volume 7) covers important advances on both experimental (preclinical) and clinical cancer research in drug development.

 

The book series offers readers an insight into current and future therapeutic approaches for the prevention of different types of cancers, synthesizing new anti-cancer agents, new patented compounds, targets and agents for cancer therapy as well as recent molecular and gene therapy research.

The topics covered in the seventh volume of this series include:

– The role of inflammation in chemotherapy-induced neuromuscular effects

– Advances in nutrigenomics and relevant anti-cancer patents

– Stimuli-responsive nanocarriers for on-demand anti-cancer drug release

– Harnessing biochemical mechanisms that control autophagy for treating esophageal cancer

 

To read out more, please visit: https://ebooks.benthamscience.com/press-releases/19012401/

Press Release | Autophagy and Mitochondria: Targets in Neurodegenerative Disorders (image)

 

Autophagy is a cellular degradation process that can cause the death of a cell in certain conditions. Autophagy is necessary to maintain cellular homeostasis by clearing out damaged cellular organelles and proteins through certain pathways. Mitochondria are cell organelles responsible for the constant supply of energy to maintain cellular physiology and energy metabolism.

Ashutosh Kumar et al. at the National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, India present a review on autophagy in neuronal cells. The researchers believe that autophagy on the neuronal cells can lead to neurodegenerative diseases and countering the effects of this process through targeted drugs can be beneficial in the fight against such diseases. Neuronal cells are more vulnerable to such bioenergetic depletion as most of their function crucially depends on availability of energy derived mainly from mitochondrial function. Any incidence of mitochondrial dysfunction inevitably results in neurodegeneration. Therefore, mitochondrial autophagy (mitophagy) plays an integral role in the onset of neurodegenerative diseases as the instance and failure of these pathways can have destructive effects on cellular homeostasis.

Previous studies show significant association between neurodegenerative disorders and mitochondrial dysfunction and abnormal mitophagy. Abnormal mitophagy leads to the accumulation of protein aggregates and consequential neurodegeneration. Future treatments for neurodegenerative disorders could involve drugs targeting mitochondria and autophagy-related proteins and enzymes. This review discusses the involvement of mitochondrial and autophagy dysfunction in neurodegenerative disorders specifically focusing on Alzheimer’s, Parkinson’s, and Huntington’s disease. Read full press release to find out more at: https://www.eurekalert.org/pub_releases/2018-12/bsp-aam122618.php

 

 

This article by Dr. Ashutosh Kumar et al. is published in CNS & Neurological Disorders – Drug Targets, Volume 17, Issue 9, 2018. The article is Open Access till 31st January, 2019. To obtain the article, please visit: http://www.eurekaselect.com/164678

eBook Highlights| Topics in Anti-Cancer Research -Volume 7

The seventh volume of the series covers topics such as drug delivery, new avenues for treatment of esophageal cancer and the role of nutrigenomics in finding new therapies.

Topics in Anti-Cancer Research covers important advances on both experimental (preclinical) and clinical cancer research in drug development. The book series offers readers an insight into current and future therapeutic approaches for the prevention of different types of cancers, synthesizing new anti-cancer agents, new patented compounds, targets and agents for cancer therapy as well as recent molecular and gene therapy research.

The comprehensive range of themes covered in each volume will be beneficial to clinicians, immunologists, and R&D experts looking for new anti-cancer targets and patents for the treatment of neoplasms, as well as varied approaches for cancer therapy.

The latest volume of the series starts with a review on non-coding RNAs and associated patents. These patents help researchers to identify various cancer biomarkers and oncogenic regulatory mechanisms. 3 chapters cover nanocarrier patents for enhanced drug delivery of chemotherapeutic agents. Nanocarriers allow drug manufacturers to encapsulate chemotherapeutic agents within thin membranes which allows the molecules to reach the targeted cellular location in the body. The specific topics refer to Nanotaxol which is a nanotechnology enhanced version of Taxol® – a chemotherapeutic agent derived from chemicals in the bark of Taxus brevifolia, stimuli responsive nanocarriers which change behavior according to temperature and pH and smart nanoformulations which rely on different chemical formulations to reach molecular targets. Other topics covered in this volume include the role of autophagy in esophageal cancer, and nutrigenomics (the science of how biological nutrients affect gene expression) in cancer research. In terms of patents, the reader will find a list of compounds which modulate autophagy, and nutrigenomic methods that allow researchers to understand nutritional biomarkers of disease and customize nutraceutical formulations based on genetic and metabolic factors, respectively. To read out more, please visit: https://ebooks.benthamscience.com/book-highlights/190102001/

 

Press Release | Cell death mechanisms in stroke and novel molecular and cellular treatment options

This article by Dr. Emine Sekerdag et al. is published in Current Neuropharmacology, Volume 16, Issue 9, 2018

 

The blood circulation to neurons is affected due to Ischemic, hemorrhagic stroke and subarachnoid hemorrhage stimulation the activation of pathophysiological responses i.e. mitochondrial death pathways, protein misfolding, apoptosis, pyroptosis, necrosis, autophagy, mitophagy, ferritinophagy, excitotoxicity, free radicals release, and inflammation. The review focuses on the recent updates in our knowledge about cellular death mechanisms caused by the loss of neuronal cells and astrocytes, damage to white matter.

Novel treatment preferences in stroke involves restoration of blood flow control and the applicability of treatments is restricted due to a limited bioactive time window of thrombolytic agents. Ischemic, hemorrhagic stroke and subarachnoid hemorrhage are discussed in this review in relation to novel molecular, cellular treatment alternatives and cellular death mechanisms.

Browse the article details at: http://www.eurekaselect.com/160188

OPEN ACCESS ARTICLE – Moving to the Rhythm with Clock (Circadian) Genes, Autophagy, mTOR, and SIRT1 in Degenerative Disease and Cancer – Current Neurovascular Research

Journal: Current Neurovascular Research

Author(s):  Kenneth Maiese

Abstract:

Background: The mammalian circadian clock and its associated clock genes are increasingly been recognized as critical components for a number of physiological and disease processes that extend beyond hormone release, thermal regulation, and sleep-wake cycles. New evidence suggests that clinical behavior disruptions that involve prolonged shift work and even space travel may negatively impact circadian rhythm and lead to multi-system disease.

Methods: In light of the significant role circadian rhythm can hold over the body’s normal physiology as well as disease processes, we examined and discussed the impact circadian rhythm and clock genes hold over lifespan, neurodegenerative disorders, and tumorigenesis.

Results: In experimental models, lifespan is significantly reduced with the introduction of arrhythmic mutants and leads to an increase in oxidative stress exposure. Interestingly, patients with Alzheimer’s disease and Parkinson’s disease may suffer disease onset or progression as a result of alterations in the DNA methylation of clock genes as well as prolonged pharmacological treatment for these disorders that may lead to impairment of circadian rhythm function. Tumorigenesis also can occur with the loss of a maintained circadian rhythm and lead to an increased risk for nasopharyngeal carcinoma, breast cancer, and metastatic colorectal cancer. Interestingly, the circadian clock system relies upon the regulation of the critical pathways of autophagy, the mechanistic target of rapamycin (mTOR), AMP activated protein kinase (AMPK), and silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1) as well as proliferative mechanisms that involve the wingless pathway of Wnt/β-catenin pathway to foster cell survival during injury and block tumor cell growth.

Conclusion: Future targeting of the pathways of autophagy, mTOR, SIRT1, and Wnt that control mammalian circadian rhythm may hold the key for the development of novel and effective therapies against aging- related disorders, neurodegenerative disease, and tumorigenesis.

Read more here: http://www.eurekaselect.com/154252

EDITOR’S CHOICE – The Hippocampal Autophagic Machinery is Depressed in the Absence of the Circadian Clock Protein PER1 that may Lead to Vulnerability During Cerebral Ischemia – Current Neurovascular Research

Journal: Current Neurovascular Research

Author(s): Abdelhaq Rami*, Julia Fekadu, Oliver Rawashdeh

Abstract:

Background: Autophagy is an intracellular bulk self-degrading process in which cytoplasmic contents of abnormal proteins and excess or damaged organelles are sequestered into autophagosomes, and degraded upon fusion with lysosomes. Although autophagy is generally considered to be pro-survival, it also functions in cell death processes. We recently reported on the hippocampal, higher vulnerability to cerebral ischemia in mice lacking the circadian clock protein PERIOD1 (PER1), a phenomenon we found to be linked to a PER1-dependent modulation of the expression patterns of apoptotic/autophagic markers.

Methods: To exclude the contribution of vascular or glial factors to the innate vulnerability of Per1 knockout-mice (Per1^−/−-mice) to cerebral ischemia in vivo, we compared the autophagic machinery between primary hippocampal cultures from wild-type (WT)- and Per1^−/−-mice, using the lipophilic macrolide antibiotic, Rapamycin to induce autophagy.

Results: Development of autophagy in WT cells involved an increased LC3-II-to-LC3-I ratio (microtubule-associated protein 1 light chain 3) and an overall increase in the level of LC3-II. In addition, immunostaining of LC3 in WT cells revealed the typical transformation of LC3 localization from a diffused staining to a dot- and ring-like pattern. In contrast, Per1^−/−-hippocampal cells were resistant to Rapamycin induced alterations of autophagy hallmarks.

Conclusion: Our in vitro data suggests that basal activity of autophagy seems to be modulated by PER1, and confirms the in vivo data by showing that the autophagic machinery is depressed in Per1^−/−-hippocampal neurons.The implication of both autophagy and circadian dysfunction in the pathogenesis of cerebral ischemia suggests that a functional connection between the two processes may exist.

Read more here: http://www.eurekaselect.com/153389

 

Most Accessed Article – Warming Up to New Possibilities with the Capsaicin Receptor TRPV1: mTOR, AMPK, and Erythropoietin – Current Neurovascular Research

Journal: Current Neurovascular Research

Author(s): Kenneth Maiese.

Abstract:

Background: Transient receptor potential (TRP) channels are a superfamily of ion channels termed after the trp gene in Drosophila that are diverse in structure and control a wide range of biological functions including cell development and growth, thermal regulation, and vascular physiology. Of significant interest is the transient receptor potential cation channel subfamily V member 1 (TRPV1) receptor, also known as the capsaicin receptor and the vanilloid receptor 1, that is a non-selective cation channel sensitive to a host of external stimuli including capsaicin and camphor, venoms, acid/basic pH changes, and temperature.

Methods: Given the multiple modalities that TRPV1 receptors impact in the body, we examined and discussed the role of these receptors in vasomotor control, metabolic disorders, cellular injury, oxidative stress, apoptosis, autophagy, and neurodegenerative disorders and their overlap with other signal transduction pathways that impact trophic factors.

Results: Surprisingly, TRPV1 receptors do not rely entirely upon calcium signaling to affect cellular biology, but also have a close relationship with the mechanistic target of rapamycin (mTOR), AMP activated protein kinase (AMPK), and protein kinase B (Akt) that have roles in pain sensitivity, stem cell development, cellular survival, and cellular metabolism. These pathways with TRPV1 converge in the signaling of growth factors with recent work highlighting a relationship with erythropoietin (EPO). Angiogenesis and endothelial tube formation controlled by EPO requires, in part, the activation of TRPV1 receptors in conjunction with Akt and AMPK pathways.

Conclusion: TRPV1 receptors could prove to become vital to target disorders of vascular origin and neurodegeneration. Broader and currently unrealized implementations for both EPO and TRPV1 receptors can be envisioned for for the development of novel therapeutic strategies in multiple systems of the body.

 

To access the article, please visit: http://www.eurekaselect.com/150838

Significant article contribution by Chinese author in the journal Current Alzheimer Research

Autophagy Enhancer Carbamazepine Alleviates Memory Deficits and Cerebral Amyloid-β Pathology in a Mouse Model of Alzheimer’s Disease

Current Alzheimer Research, 10(4): 433-441.

Author(s): Lixi Li, Sufang Zhang, Xin Zhang, Ting Li, Yu Tang, Hui Liu, Wendi Yang and Weidong Le.

Abstract: Autophagy plays an important role in Alzheimer’s disease (AD). It has been reported that autophagic flux is altered in patients with AD, and application of the autophagy enhancer rapamycin may alleviate the cognitive impairment and amyloid-β (Aβ) neuropathology in transgenic animal model of AD. Since rapamycin is also an immune suppressor, there is a concern that long-term use of rapamycin may bring severe unwanted side effects. The aim of this study is to test if carbamazepine (CBZ), an anti-epileptic drug that has a potent autophagy enhancement effect, has anti-AD effects in APP^swe/PS1^deltaE9transgenic mice model of AD. We found that APP^swe/PS1^deltaE9 mice display increased autophagic activity accompanied by decreased mTOR activity. After three months treatment with CBZ in the APP^swe/PS1^deltaE9 mice, we demonstrated that the spatial learning and memory deficits in these mice are significantly alleviated. We also documented that the cerebral amyloid plaque burden and Aβ₄₂ levels in these mice are significantly reduced. Furthermore, we showed that CBZ significantly enhances the autophagic flux in the APP^swe/PS1^deltaE9 mice which is unlikely via mTOR-dependent autophagy pathway. These data suggest that long-term CBZ treatment may have a protective effect in AD mouse model possibly through enhancing the autophagic flux.

– See more: http://benthamscience.com/journals/current-alzheimer-research/volume/10/issue/4/page/433/

 

BSP High Impact Factor Journal; Mini-Reviews in Medicinal Chemistry:

Mini-Reviews in Medicinal Chemistry:

Ranking and Category:

21^st of 59 in

Chemistry, Medicinal

Impact Factor: 3.186

Aims & Scope

The aim of Mini-Reviews in Medicinal Chemistry is to publish short reviews on the important recent developments in medicinal chemistry and allied disciplines.

The scope of Mini-Reviews in Medicinal Chemistry will cover all areas of medicinal chemistry including developments in rational drug design, synthetic chemistry, bioorganic chemistry, high-throughput screening, combinatorial chemistry, drug targets, and natural product research and structure-activity relationship studies.

Mini-Reviews in Medicinal Chemistry is an essential journal for every medicinal and pharmaceutical chemist who wishes to be kept informed and up-to-date with the latest and most important developments.

Abstracted & Indexed in:

Science Citation Index Expanded^®, Journal Citation Reports/Science Edition, ISI Alerting Services, Biochemistry & Biophysics Citation Index^®, Index to Scientific Reviews^®, MEDLINE/Index Medicus, BIOSIS, BIOSIS Previews, BIOISIS Reviews Reports and Meetings Chemical Abstracts, Scopus, EMBASE/Excerpta Medica, PubsHub, Genamics JournalSeek, Media Finder^®-Standard Periodical Directory, J-Gate.

For more details, visit: http://benthamscience.com/journal/index.php?journalID=mrmc

Contribution by Chinese Authors in BSP Journal: Current Alzheimer Research

1. Pan-Amyloid Oligomer Specific scFv Antibody Attenuates Memory Deficits and Brain Amyloid Burden in Mice with Alzheimer’s Disease

Author(s): Min Zhao, Shao-wei Wang, Yu-jiong Wang, Ran Zhang, Ya-nan Li, Ya-jing Su, Wei-wei Zhou, Xiao-lin Yu and Rui-tian Liu

Affiliation: National Key Laboratory of Biochemical Engineering, Institute of Process Engineering, Chinese Academy of Sciences, Beijing 100190, China.

Abstract

Amyloid oligomers have a critical function in the pathologic processes of various amyloidoses, such as Alzheimer’s disease (AD), Parkinson disease (PD), Huntington’s disease, prion-related diseases, type 2 diabetes, and hereditary renal amyloidosis. Our previous reports demonstrated that a conformation-dependent oligomer-specific single-chain variable fragment (scFv) antibody, W20, isolated from a naïve human scFv library, can recognize oligomers assembled from α -synuclein, amylin, insulin, A β40/42, prion peptide 106–126, and lysozyme, inhibit the aggregation of various amyloid, and attenuate amyloid oligomer-induced cytotoxicity In vitro. Furthermore, W20 recognized the amyloid oligomers in all types of plaques, Lewy bodies, and amylin deposits in the brain tissues of AD and PD patients and in the pancreas of type 2 diabetes patients. In the current study, we showed that W20 blocked the binding of Aβ oligomers to SH-SY5Y cells, did not bind to heat shock protein, rescued cognitive impairments in APP/PS1 transgenic mice, and interfered with Aβ levels and deposits in mouse brain. These results suggest that W20 may be a promising therapeutic for the treatment of AD.

 

2. Autophagy Enhancer Carbamazepine Alleviates Memory Deficits and Cerebral Amyloid-β Pathology in a Mouse Model of Alzheimer’s Disease

Author(s): Lixi Li, Sufang Zhang, Xin Zhang, Ting Li, Yu Tang, Hui Liu, Wendi Yang and Weidong Le

Affiliation: Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.

Abstract

Autophagy plays an important role in Alzheimer’s disease (AD). It has been reported that autophagic flux is altered in patients with AD, and application of the autophagy enhancer rapamycin may alleviate the cognitive impairment and amyloid-β (Aβ) neuropathology in transgenic animal model of AD. Since rapamycin is also an immune suppressor, there is a concern that long-term use of rapamycin may bring severe unwanted side effects. The aim of this study is to test if carbamazepine (CBZ), an anti-epileptic drug that has a potent autophagy enhancement effect, has anti-AD effects in APP^swe/PS1^deltaE9 transgenic mice model of AD. We found that APP^swe/PS1^deltaE9 mice display increased autophagic activity accompanied by decreased mTOR activity. After three months treatment with CBZ in the APP^swe/PS1^deltaE9 mice, we demonstrated that the spatial learning and memory deficits in these mice are significantly alleviated. We also documented that the cerebral amyloid plaque burden and Aβ₄₂ levels in these mice are significantly reduced. Furthermore, we showed that CBZ significantly enhances the autophagic flux in the APP^swe/PS1^deltaE9 mice which is unlikely via mTOR-dependent autophagy pathway. These data suggest that long-term CBZ treatment may have a protective effect in AD mouse model possibly through enhancing the autophagic flux.

 

3. Autophagy Enhancer Carbamazepine Alleviates Memory Deficits and Cerebral Amyloid-β Pathology in a Mouse Model of Alzheimer’s Disease

Author(s): Lixi Li, Sufang Zhang, Xin Zhang, Ting Li, Yu Tang, Hui Liu, Wendi Yang and Weidong Le

Affiliation: Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.

Abstract

Autophagy plays an important role in Alzheimer’s disease (AD). It has been reported that autophagic flux is altered in patients with AD, and application of the autophagy enhancer rapamycin may alleviate the cognitive impairment and amyloid-β (Aβ) neuropathology in transgenic animal model of AD. Since rapamycin is also an immune suppressor, there is a concern that long-term use of rapamycin may bring severe unwanted side effects. The aim of this study is to test if carbamazepine (CBZ), an anti-epileptic drug that has a potent autophagy enhancement effect, has anti-AD effects in APP^swe/PS1^deltaE9 transgenic mice model of AD. We found that APP^swe/PS1^deltaE9 mice display increased autophagic activity accompanied by decreased mTOR activity. After three months treatment with CBZ in the APP^swe/PS1^deltaE9 mice, we demonstrated that the spatial learning and memory deficits in these mice are significantly alleviated. We also documented that the cerebral amyloid plaque burden and Aβ₄₂ levels in these mice are significantly reduced. Furthermore, we showed that CBZ significantly enhances the autophagic flux in the APP^swe/PS1^deltaE9 mice which is unlikely via mTOR-dependent autophagy pathway. These data suggest that long-term CBZ treatment may have a protective effect in AD mouse model possibly through enhancing the autophagic flux.

 

For more details on the journal, please visit: Current Alzheimer Research