May 30, 2017 These cross-section images show three-dimensional human skin models made of living skin cells. Untreated model skin (left panel) shows a thinner dermis layer (black arrow) compared with model skin treated with the antioxidant methylene blue (right panel). A new study suggests that methylene blue could slow or reverse dermal thinning (a sign of aging) and a number of other symptoms of aging in human skin. Credit: Zheng-Mei Xiong/University of Maryland

New work from the University of Maryland suggests that a common, inexpensive and safe chemical could slow the aging of human skin. The researchers found evidence that the chemicalan antioxidant called methylene bluecould slow or reverse several well-known signs of aging when tested in cultured human skin cells and simulated skin tissue. The study was published online in the journal Scientific Reports on May 30, 2017.

"Our work suggests that methylene blue could be a powerful antioxidant for use in skin care products," said Kan Cao, senior author on the study and an associate professor of cell biology and molecular genetics at UMD. "The effects we are seeing are not temporary. Methylene blue appears to make fundamental, long-term changes to skin cells."

The researchers tested methylene blue for four weeks in skin cells from healthy middle-aged donors, as well as those diagnosed with progeriaa rare genetic disease that mimics the normal aging process at an accelerated rate. In addition to methylene blue, the researchers also tested three other known antioxidants: N-Acetyl-L-Cysteine (NAC), MitoQ and MitoTEMPO (mTEM).

In these experiments, methylene blue outperformed the other three antioxidants, improving several age-related symptoms in cells from both healthy donors and progeria patients. The skin cells (fibroblasts, the cells that produce the structural protein collagen) experienced a decrease in damaging molecules known as reactive oxygen species, a reduced rate of cell death and an increase in the rate of cell division throughout the four-week treatment.

Next, Cao and her colleagues tested methylene blue in fibroblasts from older donors (>80 years old) again for a period of four weeks. At the end of the treatment, the cells from older donors had experienced a range of improvements, including decreased expression of two genes commonly used as indicators of cellular aging: senescence-associated beta-galactosidase and p16.

"I was encouraged and excited to see skin fibroblasts, derived from individuals more than 80 years old, grow much better in methylene blue-containing medium with reduced cellular senescence markers," said Zheng-Mei Xiong, lead author of the study and an assistant research professor of cell biology and molecular genetics at UMD. "Methylene blue demonstrates a great potential to delay skin aging for all ages."

The researchers then used simulated human skin (a system developed by Cao and Xiong) to perform several more experiments. This simulated skina three-dimensional model made of living skin cellsincludes all the major layers and structures of skin tissue, with the exception of hair follicles and sweat glands. The model skin could also be used in skin irritation tests required by the Food and Drug Administration for the approval of new cosmetic products, Cao said.

"This system allowed us to test a range of aging symptoms that we can't replicate in cultured cells alone," Cao said. "Most surprisingly, we saw that model skin treated with methylene blue retained more water and increased in thicknessboth of which are features typical of younger skin."

The researchers also used the model skin to test the safety of cosmetic creams with methylene blue added. The results suggest that methylene blue causes little to no irritation, even at high concentrations. Encouraged by these results, Cao, Xiong and their colleagues hope to develop safe and effective ways for consumers to benefit from the properties of methylene blue.

"We have already begun formulating cosmetics that contain methylene blue. Now we are looking to translate this into marketable products," Cao said. "We are also very excited to develop the three-dimensional skin model system. Perhaps down the road we can customize the system with bioprinting, such that we might be able to use a patient's own cells to provide a tailor-made testing platform specific to their needs."

The research paper, "Anti-Aging Potentials of Methylene Blue for Human Skin Longevity," Zheng-Mei Xiong, Mike O'Donovan, Linlin Sun, Ji Young Choi, Margaret Ren and Kan Cao, was published online in the journal Scientific Reports on May 30, 2017.

Explore further: Safe, inexpensive chemical found to reverse symptoms of progeria in human cells

More information: Zheng-Mei Xiong et al, Anti-Aging Potentials of Methylene Blue for Human Skin Longevity, Scientific Reports (2017). DOI: 10.1038/s41598-017-02419-3

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Common antioxidant could slow symptoms of aging in human skin - Medical Xpress

Physicist Stephen Hawking is perhaps the most famous sufferer of motor neuron disease, a crippling degenerative condition that affects an estimated 150,00 people around the world.

Karwai Tang / Getty

In news that may bring hope to Stephen Hawking and hundreds of thousands of others around the world, British scientists have used reprogrammed skin cells to study the development of motor neuron disease.

Its like changing the postcode of a house without actually moving it, explains neuroscientist Rickie Patani, referring to research offering startling new insights into the progress and treatment of the crippling degenerative condition, also known as amyotrophic lateral sclerosis (ALS).

Patani, together with colleague Sonia Gandhi, both from the Francis Crick Institute and University College London, in the UK, led a team of researchers investigating how the disease destroys the nerve cells that govern muscle movement.

The results, published in the journal Cell Reports, comprise the most fine-grained work to date on how ALS operates on a molecular level and suggest powerful new treatment methods based on stem cells.

Indeed, so exciting are the implications of the research that Ghandi and Patani are already working with pharmaceutical companies to develop their discoveries.

The neurologists uncovered two key interlinked interactions in the development of motor neuron disease, the first concerning a particular protein, and the second concerning an auxiliary nerve cell type called astrocytes.

To make their findings, the team developed stem cells from the skin of healthy volunteers and a cohort carrying a genetic mutation that leads to ALS. The stem cells were then guided into becoming motor neurons and astrocytes.

We manipulated the cells using insights from developmental biology, so that they closely resembled a specific part of the spinal cord from which motor neurons arise, says Patani.

We were able to create pure, high-quality samples of motor neurons and astrocytes which accurately represent the cells affected in patients with ALS."

The scientists then closely monitored the two sets of cells healthy and mutated to see how their functioning differed over time.

The first thing they noted was that a particular protein TDP-43 behaved differently. In the patient-derived samples TDP-43 leaked out of the cell nucleus, catalysing a damaging chain of events inside the cell and causing it to die.

The observation provided a powerful insight into the molecular mechanics of motor neuron disease.

Knowing when things go wrong inside a cell, and in what sequence, is a useful approach to define the critical molecular event in disease, says Ghandi.

One therapeutic approach to stop sick motor neurons from dying could be to prevent proteins like TDP-43 from leaving the nucleus, or try to move them back.

The second critical insight was derived from the behaviour of astrocytes, which turned out to function as a kind of nursemaid, supporting motor neuron cells when they began to lose function because of protein leakage.

During the progression of motor neuron disease, however, the astrocytes like nurses during an Ebola outbreak eventually fell ill themselves and died, hastening the death of the neurons.

To test this, the team did a type of mix and match exercise, concocting various combinations of neurons and astrocytes from healthy and diseased tissue.

They discovered that healthy astrocytes could prolong the functional life of ALS-affected motor neurons, but damaged astrocytes struggled to keep even healthy motor neurons functioning.

The research reveals both TDP-43 and astrocytes as key therapeutic targets, raising the possibility that the progress of ALS might be significantly slowed, or perhaps even halted.

Our work, along with other studies of ageing and neurodegeneration, would suggest that the cross-talk between neurons and their supporting cells is crucial in the development and progression of ALS, says Patani.

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Patients' stem cells point to potential treatments for motor neuron disease - Cosmos