Anatomy and Neuroscience - Research Publications
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ItemTrends and Challenges in Biobanking(Federation Press, 2017)The last twenty years have seen the emergence of the phenomena of biobanks, which are now regarded as essential research infrastructure in most countries around the world. However, the very nature of biobanks, as long-term repositories of sample and data that are used for many different research purposes continues to challenge many of the legal requirements for medical research, both in the UK and Australia. This chapter will provide an overview of biobanking and discuss some of the legal challenges that these activities raise by discussing and comparing the UK and Australian legal landscapes.
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ItemNo Preview AvailableBlindspots and boundaries: Exploring the role and ethical responsibilities of facilitators of stem cell tourism(African Sun media, Stellenbosch, 2016)
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ItemNo Preview AvailableNon-coding RNAs: An Introduction(SPRINGER, 2016)For many years the main role of RNA, it addition to the housekeeping functions of for example tRNAs and rRNAs, was believed to be a messenger between the genes encoded on the DNA and the functional units of the cell, the proteins. This changed drastically with the identification of the first small non-coding RNA, termed microRNA, some 20 years ago. This discovery opened the field of regulatory RNAs with no or little protein-coding potential. Since then many new classes of regulatory non-coding RNAs, including endogenous small interfering RNAs (endo-siRNAs), PIWI-associated RNAs (piRNAs), and long non-coding RNAs, have been identified and we have made amazing progress in elucidating their expression, biogenesis, mechanisms and mode of action, and function in many, if not all, biological processes. In this chapter we provide an introduction about the current knowledge of the main classes of non-coding RNAs, what is know about their biogenesis and mechanism of function.
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ItemBACE Inhibition as a Therapeutic Strategy for Alzheimer’s Disease(Bentham Science eBooks, 2015-07-22)Alzheimer’s disease (AD) is the most common age-related neurodegenerative disease and the most common cause of dementia. One of the characteristic hallmarks of AD brains upon post-mortem examination is the presence of amyloid plaques containing aggregates of the neurotoxic amyloid-β peptide Aβ. This peptide is produced from the amyloid precursor protein (APP) by proteolytic cleavage, firstly by BACE1 (β-site amyloid precursor protein cleaving enzyme 1 or β-secretase) and subsequently by γ-secretase. After Phase III, clinical trials of a γ-secretase inhibitor were abandoned due to adverse secondary effects, the focus has shifted to BACE1 as a key drug target in AD. Numerous BACE inhibitors have been produced, many of which have been shown in animal models to reduce the levels of Aβ in the brain. Intensive research effort for more than a decade has seen certain BACE1 inhibitors advance through human trials. Despite this progress, however, concerns that using BACE1 inhibition to reduce Aβ could cause unwanted side-effects (termed “mechanism-based toxicity”) have arisen as the list of BACE1 substrates continues to grow. In addition to APP, recent proteomics studies have identified novel BACE1 substrates, many of which have known roles in the developing and mature brain. This chapter aims to review the BACE inhibition strategy and describe the development of BACE inhibitors for AD therapy, highlighting both the promise and the potential pitfalls of this approach. The potential consequences of inhibiting BACE1 processing of these other BACE1 substrates along with APP will be discussed.