Gabrielle Moro, Pierre-Yves Morvan, Romuald Vallée – Codif Recherche et Nature, France
ANTI-AGEING
Neuron ageing and its effect on skin homeostasis
Nerves are at the core of how skin functions. The network of nerve endings extends throughout the cutaneous layers, from the hypodermis to the deep layers of the epidermis. They play an important role in the way we perceive our environment through the sense of touch. Nerves also convey our emotions to the skin surface. Thus, tension from stress or annoyance can be manifested on the skin by redness or itching. Nerve endings also play a physiological role inside the skin. Nerves communicate with other cutaneous cells through neurotransmitters that can impact skin pigmentation, tone or the hydration rate. This latter property has been widely studied and put into use during the past few years through a discipline commonly known as neurocosmetics. Until now, nerve endings were considered pathways. It was thought that the information delivered by touch was first of all transmitted to the central nervous system and then decoded and analysed by the brain. However, in 2014, research scientists showed that information was directly decoded and analysed by the nerve fibres before being sent to the brain.1 This discovery gives new importance to the key function and place of nerve endings in skin, but also gives rise to a number of questions on the role of nerve endings in the physiological evolution of skin. We know that ageing is accompanied by a loss of sensitivity in touch. Medical research has demonstrated that this loss
ABSTRACT
Initiated in the 2000s, ‘neurocosmetics’ refers to topical ingredients that work on the cutaneous nervous system to restore the mediator-receptor balance in the epidermis. It has led to new ways of inducing a positive action on the skin’s nervous system which results in increased skin health. In 2014 scientists discovered that
our touch experiences are processed by neurons in the skin before they reach the brain for further processing. Meanwhile it has been demonstrated
that human skin loses its cutaneous sensitivity with age due to an ageing of
in sensitivity is directly related to ageing, in particular to the degeneration of nerve endings.2
What about the impact of
neuroageing on the skin itself? Could the ageing of these fibres, which are located inside the skin and are known to communicate with other types of cells, affect skin ageing? If so, how? The study of the neurodegeneration
process, especially in medical applications of the Alzheimer’s disease type, have enabled establishing the major role of a neurotoxic peptide called amyloid beta (Aβ), which forms so-called senile plaques on the surface of nerve endings (Fig. 1).3 This neurotoxic peptide comes from a membrane protein known as Amyloid
sAPPα
Formation of senile plaques
Ageing α+γ secretase APP
Figure 1: Schematic representation of the formation of senile plaques on neurons ending.
Figure 2: Schematic representation of APP processing. September 2015 PERSONAL CARE 69 β+γ secretase Aβ neurotoxic neuroprotector
sensory fibres in the skin. We know that in the dermis, fibroblasts and neurons are continuously communicating. Can ageing of sensory fibres impact fibroblasts and therefore skin youth? Working on specific nerves culture models, Codif R&N has highlighted that neuroageing leads to the release of toxic molecules that directly affect fibroblast activity. By treating this issue Neuroguard opens
the door to new neurocosmetic strategies, not only focused on neuromediators, but on the impact of neurons ageing on skin homeostasis and ageing.
Precursor Protein (APP), which is located on the neuron surface. As its name implies, this protein is a precursor that can be cleaved in two different ways. To simplify, we can describe a first type of cleavage that is triggered by a β secretase enzyme and gives rise to the liberation of neurotoxic Aβ. A second type of cleavage is triggered by the liberation of an sAPPα peptide, which, contrary to Aβ has neuroprotective properties (Fig. 2).4 These two cleavages exist in a balanced
manner within a neuronal population that could be qualified as young. Ageing, and, in a general and repetitive manner, the accumulation of oxidising stress leads to a gradual imbalance, where the cleavage
Neuron
Aβ A Aββ Aβ
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