Genetic variations in a region of our DNA called PARKIN is associated with an increased risk of developing Parkinson’s – particularly young-onset PD (diagnosed before the age of 40yrs).
This area of DNA provides the instructions for making a protein (also referred to as PARKIN), which plays a number of important roles inside of cells.
Recently, a South Korean biotech company called Cellivery has published research on an experimental therapeutic agent that easily penetrates both the brain and cells within, delivering PARKIN protein to the cells that need it.
In today’s post, we will discuss what PARKIN does, review the new research report, and explore what could happen next.
Here on the SoPD we often talk about research regarding the prominent Parkinson’s associated proteins, think of alpha synuclein, LRRK2 and GBA. And they are of interest as there is a great deal of activity now at the clinical level exploring agents targetting these proteins.
But there are a number of interesting therapeutics being developed that are exploring some of the other Parkinson’s-associated proteins.
A good example was published this week:
Title: Intracellular delivery of Parkin rescues neurons from accumulation of damaged mitochondria and pathological α-synuclein
Authors: Chung E, Choi Y, Park J, Nah W, Park J, Jung Y, Lee J, Lee H, Park S, Hwang S, Kim S, Lee J, Min D, Jo J, Kang S, Jung M, Lee PH, Ruley HE & Jo D
Journal: Science Advances, 29 Apr 2020:6, 18, eaba1193
In this study, South Korean researchers demonstrated that a brain penetrating compound (including the PARKIN protein) can rescue numerous models of Parkinson’s.
Hang on a second: What is PARKIN?
A new research report has been published this week which may point not only towards a new understanding of the biology of Parkinson’s, but also to potentially novel therapies which are clinically available.
These exciting new findings involve a DNA repair mechanism called ‘poly ADP ribose polymerase’ (or simply PARP) and a process of cell death called Parthanatos.
Biotech companies have developed PARP inhibitors which have been reported to rescue models of Parkinson’s. With a bit of tweaking, this class of drugs could potentially be re-purposed for Parkinson’s.
In today’s post, we will look at what PARP is, explain how PARP inhibitors work, review what previous PD research has been conducted on this topic, evaluate the new report, and consider what it means for the Parkinson’s community (Spoiler alert: this will be a long post!).
Ah, the good old days!
Remember them. Way back before Netflix. When life was sooo much easier.
You know what I’m talking about.
Back when biology was simple. Remember when DNA gave rise to RNA and RNA gave rise to protein, and that was it. Simpler times they were. Now, everything is so much more complicated. We have all manner of ‘regulatory RNA’, epigentics, splice variants, and let’s not get started on the labyrinthian world of protein folding.
Oh, how I long for the good old days.
Back when a cell could only die one of two ways: apoptosis (a carefully controlled programmed manner of death) and necrosis (cell death by injury):
Now life is too complicated and complex beyond reason or imagination.
Let’s just take the example of cell death that I mentioned above: over the past decade, the Nomenclature Committee on Cell Death (or NCCD – I kid you not there is actually a committee for this) has written up guidelines for the definition/interpretation of ‘cell death’. And as part of that effort they have decided that there are now at least 12 (yes, 12) different ways a cell can die:
For those of who are interested in reading more about all of these different kinds of cell death, click here to read NCCD committee’s most recent recommendations which were updated this year (2018). Some riveting betime reading.
Which form of cell death applies to Parkinson’s?
Now that’s a really good question!
One that has been studied and the source of debate for a very long time.
To be fair, we don’t really know. But fascinating new research published this week suggests that the Parthanatos pathway could be involved in the cell death associated with Parkinson’s.
What is Parthanatos?
At the Society for Neuroscience annual meeting in 2015, the results of a small phase I clinical trial were presented and the Parkinson’s community got really excited by what they saw.
The study had investigated the use of a cancer drug called ‘Nilotinib’ (also known as Tasigna) on Parkinson’s and the initial results were rather interesting.
Two larger phase II clinical trials of Nilotinib in Parkinson’s are currently being conducted, but this week preclinical research of a new drug (called Radotinib) was published. And these new findings suggest that Nilotinib may have some impressive competition.
In today’s post, we will look at what Nilotinib and Radotinib actually do, we will review the new research, and we will discuss what the findings could mean for the Parkinson’s community.
Lots of research. Source: Thedaily
Earlier this week I wrote a post highlighting research involving a new drug (NLY01; a GLP1 receptor agonist) being developed for Parkinson’s (Click here to read that post). It was an amazing amount of work and a very impressive achievement for the research group that conducted the work.
It must have taken a long time to perform the experiments, and I figured that the researchers behind the study would probably take a well earned break.
You will understand that I was a little surprised the day after publishing the post, that I woke up to find that that same research group had published another rather remarkable amount of research… on a completely different novel drug (called Radotinib) which is also being developed for Parkinson’s!!!
Basically sums my reaction. Source: Canacopegdl
The words ‘You have to be kidding me‘ actually passed across my lips as I downloaded the new research report.
And the new drug is really interesting.
It is very similar to Nilotinib.
What is Nilotinib?
In 2018, there is one particular clinical trial that I will be watching, because the drug being tested could have a big impact on certain kinds of Parkinson’s.
The clinical trial is focused on people with cancer and they will be treated with a drug called TVB-2640. TVB-2640 is an inhibitor of an enzyme called fatty acid synthase (or FAS).
In today’s post we will discuss why TVB-2640 might be a useful treatment for certain kinds of Parkinson’s.
Mitochondria and their location in the cell. Source: NCBI
Regular readers of this blog are probably getting sick of the picture above.
I use it regularly on this website, because a.) it nicely displays a basic schematic of a mitochondrion (singular), and where mitochondria (plural) reside inside a cell. And b.) a lot of evidence is pointing towards mitochondrial dysfunction in Parkinson’s.
What are mitochondria?
Mitochondria are the power stations of each cell. They help to keep the lights on. Without them, the party is over and the cell dies.
How do they supply the cell with energy?
They convert nutrients from food into Adenosine Triphosphate (or ATP). ATP is the fuel which cells run on. Given their critical role in energy supply, mitochondria are plentiful (some cells have thousands) and highly organised within the cell, being moved around to wherever they are needed.
What does this have to do with Parkinson’s?
Last week, as everyone was preparing for Christmas celebrations, researchers at the pharmaceutic company Novartis published new research on a gene that is involved with Parkinson’s, called PARKIN (or PARK2).
They used a new gene editing technology – called CRISPR – to conduct a large screening study to identify proteins that are involved with the activation of PARKIN.
In today’s post we will look at what PARKIN does, review the research report, and discuss how these results could be very beneficial for the Parkinson’s community.
As many people within the Parkinson’s community will be aware, 2017 represented the 200th anniversary of the first report of Parkinson’s disease by James Parkinson.
It also the 20th anniversary of the discovery of first genetic mutation (or variant) that increases the risk of developing Parkinson’s. That genetic variation occurs in a region of DNA (a gene) called ‘alpha synuclein’. Yes, that same alpha synuclein that seems to play such a critical role in Parkinson’s (Click here to read more about the 20th anniversary).
In 2018, we will be observing the 20th anniversary of the second genetic variation associated with Parkinson.
That gene is called PARKIN:
Title: Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism.
Authors: Kitada T, Asakawa S, Hattori N, Matsumine H, Yamamura Y, Minoshima S, Yokochi M, Mizuno Y, Shimizu N
Journal: Nature. 1998 Apr 9; 392(6676):605-8
In 1998, Japanese researchers published this report based on 5 individuals from 4 Japanese families who were affected by juvenile-onset Parkinson’s. In family 1, the affected individual was a female, 43 years old, born of first-cousin parents, and her two younger brothers are healthy. Her condition was diagnosed in her teens and it had then progressed very slowly afterwards. Her response to L-dopa was very positive, but L-dopa-induced dyskinesia were frequent. In family 2-4, affected individuals (born to unrelated parents) exhibited very similar clinical features to the subject in family 1. The age of onset was between 18 to 27 years of age.
Using previous research and various techniques the investigators were able to isolate genetic variations that were shared between the 5 affected individuals. They ultimately narrowed down their search to a section of DNA containing 2,960 base pairs, which encoded a protein of 465 amino acids.
They decided to call that protein PARKIN.
PARKIN Protein. Source: Wikipedia
How much of Parkinson’s is genetic?
In Silicon valley (California), everyone is always looking for the “next killer app” – the piece of software (or application) that is going to change the world. The revolutionary next step that will solve all of our problems.
The title of today’s post is a play on the words ‘killer app’, but the ‘app’ part doesn’t refer to the word application. Rather it relates to the Alzheimer’s disease-related protein Amyloid Precursor Protein (or APP). Recently new research has been published suggesting that APP is interacting with a Parkinson’s disease-related protein called Leucine-rich repeat kinase 2 (or LRRK2).
The outcome of that interaction can have negative consequences though.
In today’s post we will discuss what is known about both proteins, what the new research suggests and what it could mean for Parkinson’s disease.
Seattle. Source: Thousandwonders
In the mid 1980’s James Leverenz and Mark Sumi of the University of Washington School of Medicine (Seattle) made a curious observation.
After noting the high number of people with Alzheimer’s disease that often displayed some of the clinical features of Parkinson’s disease, they decided to examined the postmortem brains of 40 people who had passed away with pathologically confirmed Alzheimer’s disease – that is, an analysis of their brains confirmed that they had Alzheimer’s.
What the two researchers found shocked them:
Title: Parkinson’s disease in patients with Alzheimer’s disease.
Authors: Leverenz J, Sumi SM.
Journal: Arch Neurol. 1986 Jul;43(7):662-4.
Of the 40 Alzheimer’s disease brains that they looked at nearly half of them (18 cases) had either dopamine cell loss or Lewy bodies – the characteristic features of Parkinsonian brain – in a region called the substantia nigra (where the dopamine neurons are located). They next went back and reviewed the clinical records of these cases and found that rigidity, with or without tremor, had been reported in 13 of those patients. According to their analysis 11 of those patients had the pathologic changes that warranted a diagnosis of Parkinson’s disease.
And the most surprising aspect of this research report: Almost all of the follow up studies, conducted by independent investigators found exactly the same thing!
It is now generally agreed by neuropathologists (the folks who analyse sections of brain for a living) that 20% to 50% of cases of Alzheimer’s disease have the characteristic round, cellular inclusions that we call Lewy bodies which are typically associated with Parkinson disease. In fact, in one analysis of 145 Alzheimer’s brains, 88 (that is 60%!) had chemically verified Lewy bodies (Click here to read more about that study).
A lewy body (brown with a black arrow) inside a cell. Source: Cure Dementia
Oh, and if you are wondering whether this is just a one way street, the answer is “No sir, this phenomenon works both ways”: the features of the Alzheimer’s brain (such as the clustering of a protein called beta-amyloid) are also found in many cases of pathologically confirmed Parkinson’s disease (Click here and here to read more about this).
So what are you saying? Alzheimer’s and Parkinson’s disease are the same thing???
In October 2015, researchers from Georgetown University announced the results of a small clinical trial that got the Parkinson’s community very excited. The study involved a cancer drug called Nilotinib, and the results were rather spectacular.
What happened next, however, was a bizarre sequence of disagreements over exactly what should happen next and who should be taking the drug forward. This caused delays to subsequent clinical trials and confusion for the entire Parkinson’s community who were so keenly awaiting fresh news about the drug.
Earlier this year, Georgetown University announced their own follow up phase II clinical trial and this week a second phase II clinical trial funded by a group led by the Michael J Fox foundation was initiated.
In todays post we will look at what Nilotinib is, how it apparently works for Parkinson’s disease, what is planned with the new trial, and how it differs from the ongoing Georgetown Phase II trial.
The FDA. Source: Vaporb2b
This week the U.S. Food and Drug Administration (FDA) has given approval for a multi-centre, double-blind, randomised, placebo-controlled Phase IIa clinical trial to be conducted, testing the safety and tolerability of Nilotinib (Tasigna) in Parkinson’s disease.
This is exciting and welcomed news.
What is Nilotinib?
Nilotinib (pronounced ‘nil-ot-in-ib’ and also known by its brand name Tasigna) is a small-molecule tyrosine kinase inhibitor, that has been approved for the treatment of imatinib-resistant chronic myelogenous leukemia (CML).
What does any that mean?
Basically, it is the drug that is used to treat a type of blood cancer (leukemia) when the other drugs have failed. It was approved for treating this cancer by the FDA in 2007.
In today’s post we will review recent research regarding one particular family of bacteria, Helicobacter pylori, and what they might be doing in relations to Parkinson’s disease.
In his magnificent book, I contain multitudes, science writer/journalist Ed Yong writes that we – every single one of us – release approximately 37 million bacteria per hour. By talking, breathing, touching, or simply being present in the world, we are losing and also picking up the little passengers everywhere we go.
Reminds me of that Pascal Mercier book “Night Train to Lisbon” – We leave something of ourselves behind when we leave a place,… I’m not sure if this is what he was referring to though.
Yong also points out that: 80% of the bacteria on your right thumb are different to the bacteria on your left thumb.
It’s a fascinating book (and no, I am not receiving any royalties for saying that).
Microbes. Source: NYmag
We have discussed microbes several times on this blog, particularly in the context of the gut and its connection to Parkinson’s disease (Click here, here and here to read some of those posts). Today we are going to re-visit one particular type of microbe that we have also discussed in a previous post: Helicobacter pylori.
Helicobacter pylori. Source: Helico
Two months ago a research report was published in the scientific journal ‘Nature’ and it caused a bit of a fuss in the embryonic stem cell world.
Embryonic stem (ES) cells are currently being pushed towards the clinic as a possible source of cells for regenerative medicine. But this new report suggested that quite a few of the embryonic stem cells being tested may be carrying genetic variations that could be bad. Bad as in cancer bad.
In this post, I will review the study and discuss what it means for cell transplantation therapy for Parkinson’s disease.
For folks in the stem cell field, the absolute go-to source for all things stem cell related is Prof Paul Knoepfler‘s blog “The Niche“. From the latest scientific research to exciting new stem cell biotech ventures (and even all of the regulatory changes being proposed in congress), Paul’s blog is a daily must read for anyone serious about stem cell research. He has his finger on the pulse and takes the whole field very, very seriously.
For a long time now, Paul has been on a personal crusade. Like many others in the field (including yours truly), he has been expressing concern about the unsavoury practices of the growing direct-to-consumer, stem cell clinic industry. You may have seen him mentioned in the media regarding this topic (such as this article).
The real concern is that while much of the field is still experimental, many stem cell clinics are making grossly unsubstantiated claims to draw in customers. From exaggerated levels of successful outcomes (100% satisfaction rate?) all the way through to talking about clinical trials that simply do not exist. The industry is badly (read: barely) regulated which is ultimately putting patients at risk (one example: three patients were left blind after undergoing an unproven stem cell treatment – click here to read more on this).
While the stem cell research field fully understands and appreciates the desperate desire of the communities affected by various degenerative conditions, there has to be regulations and strict control standards that all practitioners must abide by. And first amongst any proposed standards should be that the therapy has been proven to be effective for a particular condition in independently audited double blind, placebo controlled trials. Until such proof is provided, the sellers of such products are simply preying on the desperation of the people seeking these types of procedures.
A build up of a protein called alpha synuclein inside neurons is one of the characteristic feature of the Parkinsonian brain. This protein is believed to be partly responsible for the loss of dopamine neurons in this condition.
A similar build up of alpha synuclein is also seen in the deadly skin cancer, Melanoma… but those cells don’t die (?!?)… in fact, they just keep on dividing.
Why is there this critical difference?
In today’s post we look at an interesting new study that may have solved this mystery.
A melanoma. Source: Huffington Post
Parkinson’s disease has a very strange relationship with the skin cancer melanoma.
As we have stated in previous posts (Click here, here, here and here to read those posts) people with Parkinson’s disease are 2-8 times more likely to develop melanoma than people without Parkinson’s (And this finding has been replicated a few times: Olsen et al, 2005; Olsen et al, 2006; Driver et al 2007; Gao et al 2009; Lo et al 2010; Bertoni et al 2010;Schwid et al 2010; Ferreira et al, 2010; Inzelberg et al, 2011; Liu et al 2011; Kareus et al 2012; Wirdefeldt et al 2014; Catalá-López et al 2014; Constantinescu et al 2014; Ong et al 2014).
The truly baffling detail in this story, however, is that this relationship is reciprocal – if you have melanoma you are almost 3 times more likely to develop Parkinson’s disease than someone without melanoma (Source: Baade et al 2007; Gao et al 2009).
What is melanoma exactly?
Melanoma is a type of skin cancer.
It develops from the pigment-containing cells known as melanocytes. Melanocytes are melanin-producing cells located in the bottom layer (the stratum basale) of the skin’s outer layer (or epidermis).
The location of melanocytes in the skin. Source: Wikipedia
Melanocytes produce melanin, which is a pigment found in the skin, eyes, and hair. It is also found in the brain in certain types of cells, such as dopamine neurons (where it is referred to as neuromelanin).
Neuromelanin (brown) in dopamine neurons. Source: Schatz
Melanomas are usually caused by DNA damage resulting from exposure to ultraviolet radiation. Ultraviolet radiation from tanning beds increases the risk of melanoma (Source), as does excessive air travel (Source), or simply spending to much time sun bathing.
Approximately 2.2% of men and women will be diagnosed with melanoma at some point during their lives (Source). In women, melanomas most commonly occur on the legs, while in men they are most common on the back. Melanoma makes up 5% of all cancers (Source).
Generally, melanomas is one of the safer cancers, as it can usually be detected early by visual inspection. This cancer is made dangerous, however, by its ability to metastasise (or spread to other organs in the body).
The stages of melanoma. Source: Pathophys
Are there any genetic associations between Parkinson’s disease and melanoma?
When the common genetics mutations that increase the risk of both conditions were previously analysed, it was apparent that none of the known Parkinson’s mutations make someone more susceptible to melanoma, and likewise none of the melanoma-associated genetic mutations make a person vulnerable to Parkinson’s disease (Meng et al 2012;Dong et al 2014; Elincx-Benizri et al 2014).
In fact, researchers have only found very weak genetic connections between two conditions (Click here to read our previous post on this). It’s a real mystery.
Are there any other connections between Parkinson’s disease and melanoma?
Another shared feature of both Parkinson’s disease and melanoma is the build up of a protein called alpha synuclein. Alpha synuclein is believed to be one of the villains in Parkinson’s disease – building up inside a cell, becoming toxic, and eventually killing that cell.
But recently researchers noticed that melanoma also has a build up of alpha synuclein, but those cells don’t die:
Title: Parkinson’s disease-related protein, alpha-synuclein, in malignant melanoma
Authors: Matsuo Y, Kamitani T.
Journal: PLoS One. 2010 May 5;5(5):e10481.
PMID: 20463956 (This article is OPEN ACCESS if you would like to read it)
In this study, researchers from Japan found that alpha synuclein was detected in 86% of the primary and 85% of the metastatic melanoma. Understand that the protein is not detectable in the non-melanoma cancer cells.
So what is it doing in melanoma cells?
Recently, researchers from Germany believe that they have found the answer to this question:
Title: Treatment with diphenyl-pyrazole compound anle138b/c reveals that α-synuclein protects melanoma cells from autophagic cell death
Authors: Turriani E, Lázaro DF, Ryazanov S, Leonov A, Giese A, Schön M, Schön MP, Griesinger C, Outeiro TF, Arndt-Jovin DJ, Becker D
Journal: Proc Natl Acad Sci U S A. 2017 Jun 5. pii: 201700200. doi: 10.1073/pnas.1700200114
In their study, the German researchers looked at levels of alpha synuclein in melanoma cells. They took the melanoma cells that produced the most alpha synuclein and treated those cells with a chemical that inhibits the toxic form of alpha synuclein (which results from the accumulation of the protein).
What they observed next was fascinating: the cell morphology (or physically) changed, leading to massive melanoma cell death. The investigators found that this cell death was caused by instability of mitochondria and a major dysfunction in the autophagy process.
Mitochondria, you may recall, are the power house of each cell. They keep the lights on. Without them, the lights go out and the cell dies.
Mitochondria and their location in the cell. Source: NCBI
Autophagy is the garbage disposal/recycling process within each cell, which is an absolutely essential function. Without autophagy, old proteins and mitochondria will pile up making the cell sick and eventually it dies. Through the process of autophagy, the cell can break down the old protein, clearing the way for fresh new proteins to do their job.
The process of autophagy. Source: Wormbook
Waste material inside a cell is collected in membranes that form sacs (called vesicles). These vesicles then bind to another sac (called a lysosome) which contains enzymes that will breakdown and degrade the waste material. The degraded waste material can then be recycled or disposed of by spitting it out of the cell.
What the German research have found is that the high levels of alpha synuclein keep the mitochondria stable and the autophagy process working at a level that helps to keeps the cancer cell alive.
Next, they replicated this cell culture research in mice with melanoma tumors. When the mice were treated with the chemical that inhibits the toxic form of alpha synuclein, the cancer cancer became malformed and the autophagy process was blocked.
The researchers concluded that “alpha synuclein, which in PD exerts severe toxic functions, promotes and thereby is highly beneficial to the survival of melanoma in its advanced stages”.
So what does all of this mean for Parkinson’s disease?
Well, this is where the story gets really interesting.
You may be pleased to know that the chemical (called Anle138b) which was used to inhibit the toxic form of alpha synuclein in the melanoma cells, also works in models of Parkinson’s disease:
Title: Anle138b: a novel oligomer modulator for disease-modifying therapy of neurodegenerative diseases such as prion and Parkinson’s disease.
Authors: Wagner J, Ryazanov S, Leonov A, Levin J, Shi S, Schmidt F, Prix C, Pan-Montojo F, Bertsch U, Mitteregger-Kretzschmar G, Geissen M, Eiden M, Leidel F, Hirschberger T, Deeg AA, Krauth JJ, Zinth W, Tavan P, Pilger J, Zweckstetter M, Frank T, Bähr M, Weishaupt JH, Uhr M, Urlaub H, Teichmann U, Samwer M, Bötzel K, Groschup M, Kretzschmar H, Griesinger C, Giese A.
Journal: Acta Neuropathol. 2013 Jun;125(6):795-813
PMID: 23604588 (This article is OPEN ACCESS if you would like to read it)
In this first study the researchers discovered Anle138b by conducted a large screening study to identify for molecules that could inhibit the toxic form of alpha synuclein.
They next tested Anle138b in both cell culture and rodent models of Parkinson’s disease and found it to be neuroprotective and very good at inhibiting the toxic form of alpha synuclein. And the treatment looks to be very effective. In the image below you can see dark staining of toxic alpha synuclein in the left panel from the brain of an untreated mouse, but very little staining in the right panel from an Anle138b treated mouse.
Toxic form of alpha synuclein (dark staining). Source: Max-Planck
Importantly, Anle138b does not interfere with normal behaviour of alpha synuclein in the mice (such as production of the protein, correct functioning, and eventual degradation/disposal of the protein), but it does act as an inhibitor of alpha synuclein clustering or aggregation (the toxic form of the protein). In addition, the investigators found no toxic effects of Anle138b in any of their experiments even after long-term high-dose treatment (more than one year).
And in a follow up study, the drug was effective even if it was given after the disease model had started:
Title: The oligomer modulator anle138b inhibits disease progression in a Parkinson mouse model even with treatment started after disease onset
Authors: Levin J, Schmidt F, Boehm C, Prix C, Bötzel K, Ryazanov S, Leonov A, Griesinger C, Giese A.
Journal: Acta Neuropathol. 2014 May;127(5):779-80.
PMID: 24615514 (This article is OPEN ACCESS if you would like to read it)
During the first study, the researchers had started Anle138b treatment in the mouse model of Parkinson’s disease at a very young age. In this study, however, the investigators began treatment only as the symptoms were starting to show, and Anle138b was found to significantly improve the overall survival of the mice.
One particularly interesting aspect of Anle138b function in the brain is that it does not appear to change the level of the autophagy suggesting that the biological effects of treatment with Anle138b is cell-type–specific (Click here to read more about this). In cancer cells, it is having a different effect to that in brain cells. These differences in effect may also relate to disease conditions though, as Anle138b was not neuroprotective in a mouse model of Multiple System Atrophy (MSA; Click here to read more about this).
Is Anle138b being tested in the clinic?
Ludwig-Maximilians-Universität München and the Max Planck Institute for Biophysical Chemistry (Göttingen) have spun off a company called MODAG GmbH that is looking to advance Anle138b to the clinic (Click here for the press release). The Michael J Fox Foundation are helping to fund more preclinical development of this treatment (Click here to read more about this).
We will be watching their progress with interest.
What does it all mean?
Summing up: There are many mysteries surrounding Parkinson’s disease, but some researchers from Germany may have just solved one of them and at the same time developed a potentially useful new treatment.
They have discovered that the Parkinson’s associated protein, alpha synuclein, which is produced in large amounts in the skin cancer melanoma, is actually playing an important role in keeping those cancer cells alive. By finding a molecule that can block the build up of alpha synuclein, they have not only found a treatment for melanoma, but also potentially one for Parkinson’s disease.
And given that both diseases are closely associated, this could be seen as a great step forward. Two birds with one stone as the saying goes.
The banner for today’s post was sourced from Wikipedia