ANTI-AGEING
liberating the neurotoxin becomes dominant,5
triggering the neuronal
degeneration process that we call neuroageing. The goal of the study we describe here
is to understand the impact of this phenomenon on the neuroageing of cutaneous cells, in particular the fibroblasts. Does neuroageing affect fibroblasts? Can neuroageing lead to fibroageing? After answering these questions, we will
have a look at how and why the treatment of neuroageing represents a new anti- ageing possibility for lessening wrinkles in individuals over sixty.
How neuroageing can affect fibroageing The hypothesis we are testing here is whether neurons placed under neuroageing conditions secrete messages that are potentially toxic for fibroblasts. Neuroageing was simulated by the
addition of the A factor (1 µM) to embryo cortical neurons. After 24 hours of culture, we observed a decline in viability in the
a Healthy neurons Neurons exposed to neuroageing
Fibroblasts cultivated with messengers of health neurons
Fibroblasts cultivated with messengers of neurons exposed to neuroageing
0 20 –48% 40 60 Viability (%)
Figure 3: Impact of neuroageing on neurons and fibroblasts viability. Measure of the viability of neurons cultures non exposed to Ab (Healthy neurons) and neurons exposed to 1 µm Ab for 24 hours (neurons exposed to neuroageing). The culture medium of healthy neurons is then inoculated to culture of fibroblasts (fibroblast cultivated with messengers of healthy neurons) while the culture medium of neurons exposed to Ab is inoculated to a second culture of fibroblasts (fibroblasts cultivated with messengers of neurons exposed to neuroageing).
order of 45%, thus illustrating the impact of neuroageing (Fig. 3). This neuron culture was then inoculated into human dermal fibroblast cultures, where we observed a 48% drop in fibroblast viability, as compared to fibroblast cultures receiving neuron cultures which were not exposed to neuroageing. This first result confirms the hypothesis that neurons exposed to neuroageing secrete messengers that direct impact fibroblast viability. Communication between nerves and fibroblasts becomes toxic under neuroageing conditions. The drop in viability is also accompanied by a decrease in the synthesis of collagen and elastin, respectively 86% and 81%. Therefore, neuroageing directly affects fibroageing, suggesting repercussions on global skin ageing.
b c
Protecting neurons from neuroageing To block the effects of neuroageing, Neuroguard uses a two-step strategy. First, it protects neurons from the causes of neuroageing, primarily free radicals. Used at 0.15%, Neuroguard (now referred to as ‘the new hydrolysed algin’) provides protection in the order of 42% against hydrogen peroxide toxicity on neuron viability in cultures. Next, it stimulates the neuronal
Fibroblasts cultivated with messengers of health neurons
Fibroblasts cultivated with messengers of neurons exposed to neuroageing
Figure 4: Neuroprotecting action of 0.15% Neuroguard. a) neurons not exposed to neuroageing presents healthy nuclei, visible synapses and a dendrite network which is well developed. b) neurons exposed to neuroageing with farctionated nuclei (apoptotic), thinner, shorter and fractionated dendrites with a de- structured network and synapses which are no more visible. c) neurons exposed to neuroageing + 0.15% Neuroguard recover same characteristics than healthy neurons.
70 PERSONAL CARE September 2015
Fibroblasts cultivated with messengers of neurons exposed to neuroageing and 15% Neuroguard
***p<0.001 Student’s t-test 0 50 Viability (%)
Figure 5: Protective action of 0.15% Neuroguard towards fibroaging. Measure of the viability of fibroblasts exposed to messengers released by neurons not exposed to neuroageing (healthy neurons), exposed to neuroaging (1 µm Ab for 24 hours), and exposed simultaneously to neuroageing and Neuroguard.
100 –48% ***
131% *** protection
150
synthesis of sAPPa by 87%. The neuroprotective action of sAPPa is probably due to binding of the BACE 1 receptor, which is directly involved in the inhibition of β-secretase.6
Figure 4 shows the
neuroprotective effect of the new hydrolysed algin on the neuron network. Whereas neurons which have not been exposed to neuroageing (Fig. 4) show active synapses, an extensive network and integral cell nuclei, the effect of neuroageing (Fig. 4b) is characterised by fragmented nerve endings, ‘burnt-out’ nuclei and a limited network. By stimulating the sAPPa neuroprotector, the new hydrolysed algin enables recovering the characteristics of neurons that have not been exposed to neuroageing. A complementary experiment enabled demonstrating that the protective action of the new hydrolysed algin (0.15%) on neuron viability is effective when it is used before neuroageing starts (45% protection), as well as when neuroageing is already underway (34% protection). An optimal protection of 52% is obtained when the new hydrolysed algin is used both before and after the start of neuroageing. The new hydrolysed algin is thus able to prevent and repair damage from neuroageing on nerve fibres.
80 100 120 –45%
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