Non-coding RNA were previously thought to be biologically useless molecules arising from simple transcriptional noise. These are now known to be an integral part of cellular biology and pathology. The wide range of RNA molecules have a diverse range of structures, functions, and mechanisms of action. However, structural long non-coding RNAs (lncRNAs) are a particular class of ncRNA that are proving themselves more and more important in cellular biology, as the exact structures that such RNAs form and stabilise become more understood. Nuclear Enriched Abundant Transcript 1 (NEAT1) is a specific structural RNA emerging as a critical component in the progress and development of cancer. NEAT1 forms part of multiple biological pathways, acting through a diverse group of mechanisms. The most important of these is the formation of the paraspeckle, through which it can influence the stability of a tumour to develop resistance to drugs. This review will thus cover the range of effects by which NEAT1 interacts with cancer progression in order to describe the various roles of NEAT1 in chemoresistance, as well as to identify drug targets that protein research alone could not provide.

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The rapid advancement in research technologies and bioinformatics over the past few decades has enabled researchers to shed light on the underlying mechanisms behind aging. Whilst the progress in understanding the biochemical processes involved is impressive, a lot more still needs to be uncovered before any potential effective anti-aging treatment can be produced. Unravelling the various root causes of aging is still the most important obstacle to overcome. The data available highlights that the most likely drivers of aging are the proteosome, the ribosome and telomeres. This review focuses largely on these factors and how they contribute to initiating aging and their targeting in potential therapy against the multitude of age-associated disorders. The investigation thus far of these causative factors will be presented. Understanding these root causes and how they cause aging is fundamental to present a way forward, such that the biochemical basis of aging can be discovered, in order to usher in a new wave of therapeutics against complex diseases.

Aging is becoming one of the biggest burdens to the developed world, mainly due to it being linked to a variety of diseases from neurodegenerative disorders such as Alzheimer’s disease to cancer. It involves the dysregulation of virtually every biological process known, affecting every organ and tissue by distinct mechanisms, the nature of which is only now beginning to be truly understood. This is also true for memory loss, which is considered one of the most typical signs of old age. This is not surprising, given the still limited knowledge regarding how memories and thoughts are stored and utilised by the Central Nervous System (CNS). A potential hint, however, is the recent discovery that the complement system plays a role in synaptic pruning, which is essential for erasing unneeded memories. This is particularly intriguing given that the complement system is a branch of the innate immune system which has been documented as being overactive with aging. This review will thus cover what is currently known about the relationship between the immune system and aging and how the changes in the immune system with age affect the brain in an effort to direct further research. This topic has not been reviewed as a whole, which is why this paper aims to summarise the information on this topic whilst also elaborating on the gaps in research in order to develop potential therapies for neurodegeneration and immunosenescence.