MARINE INGREDIENTS
Anti-ageing magnesium mineral complex
Brian Fitzpatrick –Oriel Marine Research & Development; Andrea Mitarotonda, Sara De Mattia - ME&theCHEMIST; Bernard Degryse, Ronan P. Murphy - Dublin City University
The intriguing question of how we age has been of major interest and as well as coming under intense scrutiny in the past decade. This is largely because we are experiencing a shifting and evolving ageing demographic. Currently, 11% of the world’s population
is over 60 years old. As we enjoy improved lifestyle, living conditions and nutrition, along with advanced medical technologies and therapeutics, this population is projected to increase to 22% by 2050. Concomitantly, life span has been
steadily rising, and modelling studies have demonstrated that life expectancy is projected to exceed 90 years by 2030. However, this does not necessarily translate into an ‘ageing well’ paradigm. This phenomenon has given rise to an increase in age-related illnesses, which in turn incurs a significant socio-economic effect and burden. As a result, intense research at the basic,
translational and clinical levels is being focused on the cellular, molecular, physiological and epigenetic mechanisms that underpin the ageing process, with the goal of increasing a person’s ‘disease free years’.
How we age At a fundamental level, ageing is defined as the gradual and accumulative loss of physiological integrity and the consequent functional impairment of tissue and organs. Thus, it is considered a determinant of a species’ lifespan. Ageing is not a simple biological process but one that begins at birth and continues throughout the entire lifespan. This process differs considerably between individuals and indeed between species. The rate and trajectory of an individual’s ageing process is defined as a biological clock, as opposed to the familiar chronological one. Paradoxically, ageing has some positive
effects, which include the prevention of certain cancers, maintaining tissue stability, guiding surrounding cells in the tissue repair process and in immune response to pathogens, through signalling molecules known as senescence- associated secretory phenotypes (SASPs), essentially acting as a guardian of homeostasis. It stands to reason that the interplay and balance between physiological and pathological roles of SASPs have been the subject of intense research. However, ageing is not a uniform process across different organ systems. Physiological ageing of an organism
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results from the cumulative and integrative ageing of tissues, with cellular ageing being the fundamental basis. This is defined as cellular senescence, of which there are many hallmarks. Our understanding of this ageing phenomenon has been limited by the fact that the cellular phenotype associated with senescence is highly variable and heterogeneous. Senescent cells show common hallmarks, but the molecular mechanisms behind these marks are not widely conserved among all the senescence pathways. This lack of universal-specific markers is a major limitation for the identification and the targeting of senescent cells both in vitro and in vivo. However, with challenge comes opportunity,
and understanding senescent pathways in dermal cells may provide novel targets for the cosmetic and health industry. The common hallmark of cellular senescence
associated with ageing is typically defined as the cessation of the cell cycle. This state of irreversible cell cycle arrest is induced by various stressors, including telomere shortening, oxidative stress, and DNA damage. SASPs are characterized by the secretion of
pro-inflammatory cytokines, growth factors, and matrix metalloproteinases. However, cells such as dermal cells can also enter a senescent state independent of telomere shortening, and this is known as premature ageing. This usually results from changes in the local microenvironment
(e.g. extracellular matrix composition) and various pathological factors, such as DNA damage, oxidative stress and various exposome stressors e.g. UV exposure and pollution, a phenomenon known as stress-induced premature senescence or SIPS. Another major biological factor in the
aetiology of ageing is ‘sterile inflammation’, otherwise termed inflammageing. Central to this process are novel inflammatory pathways known as the Damage Associated Molecular Pattern (DAMP) network. DAMPs are molecules within cells that are a component of the innate immune response released from damaged or dying cells due to trauma or an infection by a pathogen. They are also known as danger signals and alarmins because they serve as warning signs to alert the organism to any damage or infection to its cells. DAMPs are endogenous molecules released by stressed, damaged, or dying cells. They act as danger signals that alert the immune system, triggering inflammatory and repair responses. Once a DAMP is released from the cell,
it promotes a non-infectious inflammatory response by binding to a pattern recognition receptors (PRR) such as toll-like receptors (TLRs) and NOD-like receptors (NLRs), leading to the activation of innate immunity. There is accumulating evidence which indicates that ageing is associated with a
May 2025 PERSONAL CARE
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