Researchers are building as ever increasing amount of evidence supporting the idea that as our bodies age, there is an accumulation of cells that cease to function normally. But rather than simply dying, these ‘non-functional’ cells shut down and enter a state which is refered to as ‘senescence‘.
And scientists have also discovered that these senescent cells are not completely dormant. They are still active, but their activity can be of a rather negative flavour. And new research from the
The good news is that a novel class of therapies are being developed to deal with senescent cells. These new drugs are called senolytics.
In today’s post, we will discuss what is meant by senescence, we will review the new data associated with Parkinson’s, and we will consider some of the interesting senolytic approaches that could be useful for PD.
This is not my living room… honest. Source: Youtube
Humans being are great collectors.
We may not all be hoarders – as in the image above – but everyone has extra baggage. Everybody has stuff they don’t need. And the ridiculous part of this equation is that some of that stuff is kept on despite the fact that it doesn’t even work properly any more.
The obvious question is:
Oh, and don’t get me wrong – I’m not talking about all that junk you have lying around in your house/shed.
No, I’m referring to all the senescent cells in your body.
Huh? What are senescent cells?
The adult human body is made up of approximately 37 trillion cells (ball part figure – give or take around a couple of billion – Source). Of these, between 50-70 billion cells die and are generally replaced each and every day in an average adult (Please note: With 86,400 seconds in a day, that is a replacement rate of 55,000 cells per second! WOW!).
Growth of different types of cells in the body. Source: BusinessInsider
Admittedly, the bulk of those cells being replaced are in the blood, skin and intestines.
But you have to agree that it is still an incredibly high amount of turn over.
And each time each of those cells divide, something could potentially go wrong resulting in one of those millions of cells starting to multiply unchecked and uncontrollably (aka cancer).
It is rather miraculous really – just think of all the trillions of cells that have come and gone during your entire life time – just one of them needed to go rogue and hey-presto: cancer.
Mother nature seems to be a little more concerned about this situation than we are though, and she has planned ahead by bestowing us with many different anti-cancer systems which help to prevent any silly ‘rogue’ cell ambitions. These anti-cancer measures range from programmed cell death mechanisms (like apoptosis), to simply shutting cells down and making them dormant.
Que? What do you mean “shutting cells down and making them dormant”?!?
Yes, this is that “extra baggage” I was referring to in the introduction.
As we age, our bodies collect – or there is a general increase in the number of – senescent cells.
Senescence is recognised as a cellular program that induces a stable cell growth arrest, meaning that it is a system of stopping cells from dividing. Historically, senescence has been viewed as an irreversible cell-cycle halting mechanism, which functions to protect us against cancer. But more recently this idea has evolved, as a result of discoveries that have extended the role of cellular senesence away from just stopping dividing cells to include more complex biological processes, from influencing development and tissue repair all the way throught to ageing and age-related conditions (like Parkinson’s).
For one thing, it is now apparent that non-dividing cells can become senescent.
For example in the brain, different types of non-dividing cells (like neurons) have been found to be in a state of senescence. And these different types of cells becoming senescent can influence the activity of the remaining still-functional cells. As the image below suggests, when astrocytes become senescent, there is reduced support for neurons:
But how can dormant senescent cells influence their surroundings?
By releasing chemicals which can influence the world around them… and not always in the most positive way. The release of such chemicals by senescent cells means that those cells have acquired a senescence-associated secretory phenotype (or SASP).
SASP is a state where the cell is no longer doing what it is supposed to normally be doing, and it has effectly shut down. But it is still releasing chemicals that send messages to the world around it. And as I suggested above, some of those messages are not helpful.
For example, as we age, the SASP is believed to be at least partially responsible for some of the chronic inflammation associated with the aging process (also known as ‘inflammaging’), which contributes to multiple age-related conditions. Inflammation is the immune system’s response to problems in the body, and by senescent cells continuously sending negative ‘pro-inflammatory’ messages out, the immune system is kept very busy.
Click here for a very good OPEN ACCESS review of senescence in ageing.
Ok, but what does any of this have to do with Parkinson’s?
Several years ago, some researchers at the Mayo Clinic College of Medicine (Rochester, Minnesota) reported something interesting about senescent cells: they shorten the life span of mice.
Title: Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders.
Authors: Baker DJ, Wijshake T, Tchkonia T, LeBrasseur NK, Childs BG, van de Sluis B, Kirkland JL, van Deursen JM.
Journal: Nature. 2011 Nov 2;479(7372):232-6.
PMID: 22048312 (This article is OPEN ACCESS if you would like to read it)
In this study, the scientists genetically engineered a mouse that would get rid of all senescent cells from all of the organs in the body (throughout life). When they compared these mice to normal mice, the investigators found that life-long removal of cells producing high levels of p16Ink4a delayed the onset of many age-related complications. Regular elimination of senescent cells from mice resulted in the animals remained youthful longer, based on measures of their mobility, muscle mass, and fat storage.
Subsequent research has suggested that the number of astrocytes with high levels of senescence proteins actually increases in the human brain during the normal ageing process (Click here to read more about this). This phenomenon has also been observed in the brains people with Alzheimer’s:
Title: Astrocyte senescence as a component of Alzheimer’s disease.
Authors: Bhat, R., Crowe, E.P., Bitto, A., Moh, M., Katsetos, C.D., Garcia, F.U., Johnson, F.B., Trojanowski, J.Q., Sell, C., Torres, C.
Journal: PLoS ONE, 2012; 7: e45069
PMID: 22984612 (This article is OPEN ACCESS if you would like to read it)
In this study, the researchers looked at levels of two proteins associated with senescence (metalloproteinase-1 (or MMP-1) and p16INK4a) in astrocytes in fetal, middle aged (35 to 50 years) and elderly (78 to 90 years) brain tissue samples. Compared with the fetal tissue samples, the investigators observed a significant increase in the number of astrocytes with high levels of these two proteins. And this number increased when the researchers looked at elderly brains. In addition, samples from people who passed away with Alzheimer’s harboured a significantly greater level of p16INK4a-in astrocytes compared with samples from normal-healthy adult control subjects of similar ages.
What are astrocytes?
Astrocytes (Astro from Greek astron = star and cyte from Greek “kytos” = cavity but also means cell) are star-shaped cells in the brain that play a critical role in maintaining the carefully balanced environment and provide support to the other types of cells. While neurons get all of the attention because they are the cells sending messages to different parts of the brain, astrocytes are very busy working in the background, holding the show together.
Understand that without astrocytes, the wheels on the wagon would come off very quickly.
An astrocyte (green) supporting other cell types. Source: Sciencenewsforstudents
Astrocytes are some of the hardest working cells in the brain. They really regulate a lot of what is happening up there, from modulating synaptic transmission (the passing of signals from neuron to neuron) and soaking up excess neurotransmitters (the chemicals that pass the signal from neuron to neuron, such as dopamine) to responding to injury in the brain (by forming the ‘glial scar’).
A human astrocyte. Source: Wikipedia
Is there any evidence that senescent astrocytes are involved in Parkinson’s?
Earlier this year, this report was published:
Title: Cellular Senescence Is Induced by the Environmental Neurotoxin Paraquat and Contributes to Neuropathology Linked to Parkinson’s Disease
Authors: Chinta SJ, Woods G, Demaria M, Rane A, Zou Y, McQuade A, Rajagopalan S, Limbad C, Madden DT, Campisi J, Andersen JK.
Journal: Cell Rep. 2018 Jan 23;22(4):930-940.
PMID: 29386135 (This article is OPEN ACCESS if you would like to read it)
In this study, the scientists found an increase in the number of astrocytes exhibiting high levels of proteins associated with senescence in the brains of people with Parkinson’s, supporting the idea of a possible role for senescent cell burden in neurodegenerative conditions.
Of particular interest, the inviestigators found evidence of senescence biomarkers in astrocytes in the substantia nigra (the region of the brain where the dopamine-producing neurons reside – the dopamine cells being a population badly affected by PD). For example, reduced levals of a protein called lamin B1 in cells is believed to be a marker of senescence. The less lamin B cells have, the more senescent they are. And in this study, the researchers found that many astrocytes in the Parkinsonian brain were lacking lamin B1 (while no significant difference was detected in aged-matched control tissues).
You can see an example of this result in the image below: blue staining indicates the nucleus of cells, red staining denotes astrocytes, and green staining labels lamin B1. Note the lack of green staining where the red astrocyte should be in bottom right panel (from the Parkinson’s sample; indicated by a red arrow) even though the nucleus of the neighbouring cell still has lamin B1 protein (green; indicated by a yellow arrow).
Next the researchers sought to determine if chemicals associated with increasing the risk of developing Parkinson’s could also induce cellular senescence in human astrocytes. They selected the herbicide paraquat for this analysis, and they found that after exposing astrocytes grown in cell culture to paraquat, there was a robust increase in levels of proteins associated with senescence. They also found that low but sustained doses of paraquat increased the percentage of senescent astrocytes over time, suggesting that even low exposures to such a chemical over time could have an impact.
For their next experiment the investigators grew dopamine neurons in the cell culture solution which had been previously used to support senescent astrocytes and they found a significant reduction in the viability of dopamine neurons (compared to a control group of dopamine neurons that they grew in normal solution). This suggested that the senescent astrocytes were releasing certain compounds into their surrounding environment that could be having a negative impact (even after the solution is transferred to a different set of cells).
The investigators then used genetically engineered mouse in which senescent cells are automatically killed off (similar to the study mentioned further above). They began exposing these mice (and some normal control mice) to a continuous low dose of paraquat, which increased levels of senescence-associated protein p16INK4a in the substantia nigra (the region where the dopamine neurons live).
A lab mouse. Source: USNews
When they looked at dopamine neurons in the genetically engineered mice, the investigators found that the removal of senescent cells reduced the levels of dopamine cell loss associated with paraquat treatment (compared to normal mice given the same toxin). Thus, the researchers concluded that “therapies that target senescent cells may constitute a strategy for treatment of sporadic Parkinson’s, for which environmental exposure is a major risk factor”.
Wow. So astrocytes can become senescent in Parkinson’s? What about dopamine neurons? Can they become senescent?
Very recently, researchers at the Rockfeller University have made a manuscript available on BioRxiv which suggests ‘yes, dopamine cells can become senescent’:
Title: Loss of SATB1 Induces a p21 Dependent Cellular Senescence Phenotype in Dopaminergic Neurons
Authors: Riessland M, Kolisnyk B, Kim TW, Cheng J, Ni J, Pearson JA, Park EJ, Dam K, Acehan D, Ramos-Espiritu LS, Wang W, Zhang J, Shim J-W, Ciceri G, Brichta L, Studer L, Greengard P.
DOI: https://doi.org/10.1101/452243 (This manuscript is OPEN ACCESS if you would like to read it)
In this study, the researchers were interested in a protein called SATB1.
What does SATB1 do?
Special AT-rich Sequence Binding Protein 1 (or SATB1) is a DNA binding protein that plays a role in many aspects of cell activity, but in 2015 these same researchers found that it is involved in the neurodegeneration:
Title: Identification of neurodegenerative factors using translatomeregulatory network analysis.
Authors: Brichta L, Shin W, Jackson-Lewis V, Blesa J, Yap EL, Walker Z, Zhang J, Roussarie JP, Alvarez MJ, Califano A, Przedborski S, Greengard P.
Journal: Nat Neurosci. 2015 Sep;18(9):1325-33.
PMID: 26214373 (This report is OPEN ACCESS if you would like to read it)
In this study, the researchers reported that SATB1 was involved in the neurodegeneration of dopamine neurons in mouse models of Parkinson’s. When they removed this protein from dopamine neurons in mice, it resulted in those neurons dying in a similar fashion to the cells being treated with a neurotoxin.
But in their new, more recent manuscript, those same researchers reported that the dopamine cells with reduced levels of SATB1 protein were not necessarily dying because of cell death, but rather the loss of SATB1 was resulting in the dopamine neurons becoming senescent. And interestingly, this effect was specific to the dopamine neurons, as cortical neurons exhibited other effects from the loss of SATB1, but they were still viable.
The researchers found that when they removed SATB1 from embryonic stem cells, and then grew those cells into dopamine neurons, the cells missing SATB1 failed to fully develop into mature dopamine neurons. Compared to normal dopamine neurons, the cells missing SATB1 had shorter branches and struggled to survive beyond 60 days in cell culture.
When they further investigated the biology of the dopamine neurons missing SATB1, they found that they presented many of the classical features of cellular senescence (such as SASP and reduced levels of Laminin B – described above) in the dopamine neurons.
The researchers also found that dopamine neurons lacking SATB1 had impaired lysosomal and mitochondrial function.
Lysoso and mito what?
Lysosomes are small bags of digestive enzymes that can be found inside cells. They help to break down proteins that have either been brought into the cell or that have served their function and need to be digested and disposed of (or recycled).
How lysosomes work. Source: Prezi
Inside the lysosomes are enzymes which help to break material down into useful parts. The lysosome will fuse with other small bags (called vacuole) that act as storage vessels of material inside a cell. The enzymes from the lysosome will mix with the material in the vacuole and digest it (or it break down into more manageable components). Issues with lysosomal function are believed to be involved with certain aspects of Parkinson’s, perhaps resulting in the build up of clustered/aggregated proteins in the cell.
And mitochondria – you may recall from previous SoPD posts – are the power stations of each cell. They help to keep the lights on. Without them, the party is over and the cell dies.
Mitochondria and their location in the cell. Source: NCBI
You may remember from high school biology class that mitochondria are tiny bean-shaped objects within the cell. 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.
And the researchers had discovered that dopamine neurons lacking SATB1 had issues with their lysosomal and mitochondrial functions.
Interesting, but how was the absense of SATB1 causing senescence to occur in dopamine neurons?
The investigators next sought to determine why the absense of SATB1 would lead dopamine neurons to become senescent, and they found that SATB1 binds a region of DNA controlling a gene called CDKN1A. They also noted that CDKN1A levels in dopamine neurons with no SATB1 were higher than normal dopamine neurons, which led them to think that SATB1 was repressing levels of CDKN1A. In the absense of SATB1, CDKN1A levels increased, leading to the dopamine neuron becoming senescent.
The researchers completed their study by evaluating the loss of SATB1 in rodents and found that 2 weeks after reducing SATB1 levels in dopamine neurons, the cells exhibited many of the signs of senescence. In addition, there was an increase in the levels of activation of microglial cells – the resident immune cells – which become activated when dopamine cells are not well or dysfunctional.
The investigators also looked for markers of senescence in dopamine neurons on sections of postmortem brain tissue from people who had passed away with (or without) Parkinson’s, and they found a significant increase in those markers in the PD brains (compared to control brains).
Has SATB1 ever been associated with Parkinson’s before?
Yes, it has.
In a study published last year (2017), genetic variations in SATB1 were found to be associated with a higher risk of developing Parkinson’s:
Title: A meta-analysis of genome-wide association studies identifies 17 new Parkinson’s disease risk loci.
Authors: Chang D, Nalls MA, Hallgrímsdóttir IB, Hunkapiller J, van der Brug M, Cai F; International Parkinson’s Disease Genomics Consortium; 23andMe Research Team, Kerchner GA, Ayalon G, Bingol B, Sheng M, Hinds D, Behrens TW, Singleton AB, Bhangale TR, Graham RR.
Journal: Nature Genet. 2017 Oct;49(10):1511-1516.
PMID: 28892059 (This report is OPEN ACCESS if you would like to read it)
In this study, the researchers conducted a GWAS comparing DNA from 6,476 people with Parkinson’s with DNA from 302,042 controls. They then compared those results with another GWAS dataset from a recent study involving 13,000 people with Parkinson’s and 95,000 controls.
Wait a minute. What is a GWAS?
A genome-wide association study (or GWAS) is an analysis of a set of genetic variants across the entire genome (or all of the DNA in your cells, including mitochondrial), and this analysis is conducted in a large pool of different individuals to see if any variants are associated with a particular trait (or medical condition). It is typically an analysis of single nucleotide polymorphisms (or SNPs; a variation in a single nucleotide). The researcher will check your DNA for the presence of a large set of single nucleotide variations, and then compare them with the results collected from other people.
We all have these tiny genetic mutations, but what a GWAS does, is seek to determine whether people with a particular trait (for example, people with red hair) have a shared single nucleotide polymorphisms, compared to people that do not have that trait. A GWAS analysis of red haired people would point towards a variation on chromosome 16 (in the MC1R gene).
After looking at the results of both datasets, this 2017 study found that SATB1 was associated with a higher risk of developing Parkinson’s, which (given the new senescence data) begs the question of whether people with SATB1 genetic variants have a “senescence-based” form of Parkinson’s.
Obviously this question requires further research before we jump to any conclusions, but a more recent analysis of the genetics of Parkinson’s has also found variants in the SATB1 gene to be a risk factor for PD (Click here to read more about that study).
Interesting. Are there any treatments being developed for senescent cells?
Yes, there are.
They are being referred to as senolytics – a combination of the words “senescence” and “lytic” which means ‘destroying’).
Several companies are seriously investigating senolytics. In particular, a small biotech company called Unity biotechnology.
And this company seems to be very serious about moving forward with treatments that selectively target senescent cells (the management team of Unity biotechnology have collectively taken 91 therapeutic candidates into human clinical trials and they are responsible for the creation of 13 FDA-approved medicines – like I said, serious) and they have some serious money backing them (Amazon boss Jeff Bezos’ venture fund Bezos Expeditions and PayPal co-founder Peter Thiel’s Founders Fund are investors – again: serious). Currently the company has pre-clinical programs for inflammatory joint diseases and ophthalmology, but they are certainly exploring other conditions and Parkinson’s is hopefully one of them in the wake of this current research report.
And Unity biotechnology are not alone in this area of targeting cellular senescence. Oisin biotechnology are another company designing at such therapies.
And there are certainly many different avenues to explore with regards to therapeutic options for senescent cell-based complications. For example, pro-senescence therapies could be considered for cancer (forcing cancer cells to stop dividing):
Options for senescence cell therapies. Source: Researchgate
To be completely fair, this is rather blue sky research (with clinical applications still some ways off in the future), but it is a very interesting idea and major biotech firms are certainly having a good hard look at it.
And all this effort could be of particular interest to Parkinson’s.
You see, earlier this year, this research report was published:
Title: Senolytics improve physical function and increase lifespan in old age.
Authors: Xu M, Pirtskhalava T, Farr JN, Weigand BM, Palmer AK, Weivoda MM, Inman CL, Ogrodnik MB, Hachfeld CM, Fraser DG, Onken JL, Johnson KO, Verzosa GC, Langhi LGP, Weigl M, Giorgadze N, LeBrasseur NK, Miller JD, Jurk D, Singh RJ, Allison DB, Ejima K, Hubbard GB, Ikeno Y, Cubro H, Garovic VD, Hou X, Weroha SJ, Robbins PD, Niedernhofer LJ, Khosla S, Tchkonia T, Kirkland JL.
Journal: Nat Med. 2018 Aug;24(8):1246-1256.
In this study, the researchers injected mice with senescent cells and looked to see what kind of impact they had on the animals. Remarkably, the investigators found that transplanting a relatively small number of senescent cells into young mice was sufficient to cause not only physical dysfunction, but also cellular senescence other cells in the mouse. The senescent cells reduced the overall survival of the injected mice, which (the researchers suggested) demonstrated “the potency of senescent cells in shortening health- and lifespan”.
Of particular interest, however was a drug cocktail that the investigators used to try and clear the senescent cells. They used a combination of Dasatinib and Quercetin, and they found that this treatment resulted in the “selective elimination of senescent cells”, and it also decreased the number of naturally occurring senescent cells as well as their proinflammatory secretions in cultured human tissue. In addition, intermittent oral administration of this cocktail (both to senescent cell-transplanted mice and normally aged mice) rescued physical dysfunction and increased overall survival (by 36%!).
Wow! What are Quercetin and Dasatinib?
Quercetin is a plant pigment (flavonoid), which is found in many plants and foods, such as red wine, onions, green tea, etc. The researchers do not believe it is a senolytic, but it serves to enhance the senolytic properties of the second drug: Dasatinib.
Dasatinib. Source: Wikipedia
Dasatinib (sold under the brand name Sprycel) is a BRC-ABL inhibitor that is used in the treatment of chronic myeloid leukemia (CML) – a kind of blood cancer.
And for anyone who has been following Parkinson’s research for the last few years, alarm bells should be ringing.
One of the most anticipanted set of clinical trials currently being conducted for Parkinson’s focuses on a drug called Nilotinib, which is also a BRC-ABL inhibitor (Click here to read a previous SoPD post on this topic and click here to learn more about Dasatinib). The fact that Dasatinib is being used to clear senescent cells does kind of beg the question: Could Nilotinib do the same thing???
Admittedly, Dasatinib (made by Bristol-Myers Squibb) does differ from Nilotinib in that it is also an active inhibitor the Src family of tyrosine kinases (which Nilotinib does to a much less extent). But it would certainly be interesting for someone in the PD research community to have a look-see if Nilotinib and Quercetin have any combined impact on senescence.
Rockefeller University? You reading this?
Are there any clinical trials for dasatinib and quercetin?
Researchers at the Mayo Clinic in Rochester (Minnesota) have been conducting a Phase II clinical trial assessing the effect of senescent cell clearance on physical ability and mesenchymal stem cell functionality in patients with chronic kidney disease. The study involves 20 participants who will be randomly assigned to two groups: observational controls or treatment (with dasatinib and quercetin). The study is expected to report in 2021 (Click here to read more about this study).
Oh, and if dasatinib and quercetin fail to demonstrate any effect on senescent cells in humans, not to worry.
There are a number of other senolytics already being proposed.
For example, just last month this report was published:
Title: Fisetin is a senotherapeutic that extends health and lifespan.
Authors: Yousefzadeh MJ, Zhu Y, McGowan SJ, Angelini L, Fuhrmann-Stroissnigg H, Xu M, Ling YY, Melos KI, Pirtskhalava T, Inman CL, McGuckian C, Wade EA, Kato JI, Grassi D, Wentworth M, Burd CE, Arriaga EA, Ladiges WL, Tchkonia T, Kirkland JL, Robbins PD, Niedernhofer LJ.
Journal: EBioMedicine. 2018 Oct;36:18-28.
PMID: 30279143 (This report is OPEN ACCESS if you would like to read it)
In this study, the researchers evaluated 10 flavonoids for their senolytic properties, to determine if they could improve upon quercetin. Curcumin and Fisetin stood out in the analysis for their potential to reduce the number of senescent cells in cell culture.
What are curcumin and Fisetin?
Curcumin is an active component of turmeric (Curcuma longa), a dietary spice used in Indian cuisine and medicine.
Tumeric. Source: Cerebrum
Curcumin exhibits antioxidant, anti-inflammatory and anti-cancer properties, crosses the blood-brain barrier and there are numerous studies that indicate neuroprotective properties in various models of neurological disorders.
It has also been shown to prevent the aggregation of alpha synuclein (click here for more on this).
Fisetin is a flavonoid (a natural compound similar to quercetin) present in many fruits and vegetables (including apples, persimmon, grapes, onions, etc), which suggests that it is imminently translatable.
Sources of Fisetin. Source: Sciencedirect
Fisetin treatment in this recent study was found to extend the health and lifespan in normal mice, even when treatment was initiated in aged animals. And there is a building body of research to suggest that fisetin can be beneficial in neurotoxic models of Parkinson’s (Click here, here, here and here to read examples of this). It would be interesting to see what it can do in alpha synuclein models of PD.
All of this said, there is a great deal of research currently focused on senolytics and you can be sure that we will be re-addressing this topic in future SoPD posts.
So what does it al mean?
Wow, long post.
So much for my promise to shorten these rants.
But I hope you will agree that the research on senescent ‘zombie’-like cells is interesting, particularly as it could have important implications for Parkinson’s. And there is a lot to support the idea of senescent cells having an influence on PD.
Multiple research groups have recently discovered that cells in the brain have the ability to become dysfunctional with age, taking on a dormant like state that can have negative influences on their surrounding environment. There is evidence to suggest that these processes coud be affecting neurodegenerative conditions like Parkinson’s.
The good news is that there are numerous biotech companies focused on developing therapies that address these senescent cells, and it will be interesting to see if they have any potential in the battle against Parkinson’s.
As I suggested above, watch this space!
Addendum – 14/11/2018
More research on fisetin and curcumin today – Salk Institute researchers have announced the development of derivatives of these compounds, and they found that mice and flies treated with some of those derivatives not only had reduced biomarkers of ageing, but also had a longer median lifespans (Click here to read more about this new research).
Abrexa Pharmaceuticals is moving one of the derivatives (J147) into clinical trials for Alzheimer’s next year.
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