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  1. #11
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    Is there anyway you think we could apply this knowledge toward something, such as figuring a way out to stop cellular senescence Swooping? Thanks for the info, it helps me cope with my hair loss when I learn how something occurs.

  2. #12
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    Quote Originally Posted by Swooping View Post
    RU58841 isn't able to block all DHT;



    I guess that answers your question already. As you get older your cells get more susceptible to senescence too so that is why current treatments can "fail" for anyone over time.

    Yes senescence can get accompanied by inflammatory factors this is called SASP, however this doesn't have to be always the case. Senescence can occur without inflammation too. Obviously we know there are inflammatory factors present in AGA though. Like you say shedding definitely isn't a good indicator, but I think itching isn't too. You may get rid of the itching by using a corticosteroid or a other anti-inflammatory but that won't stop AGA for example. Hope that answered your questions.

    This video goes with this all too;

    Thanks for answering and for the vid, you're the man!

  3. #13
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    Hello Swooping I read some of those posts. They were really informative although some of it went over my head (specifically the part about the pathways that drive the cellular senescence in DP cells) however you posted links to th studies for everything you wrote and I appreciate it.

    Now, you are definitely onto something,.. However it seems to me it is easier to replace the senescent cells rather than trying to block the pathways that are causing the senescence. That is why I am also hopeful about Replicel, however I am still questioning their effectiveness.

    Quote Originally Posted by Kudu View Post
    Is there anyway you think we could apply this knowledge toward something, such as figuring a way out to stop cellular senescence Swooping? Thanks for the info, it helps me cope with my hair loss when I learn how something occurs.
    Hmm yes this question presents itself however I don't think we can figure out on our own how to block all the pathways responsible, that doesn't mean we shouldn't try.

  4. #14
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    Quote Originally Posted by Kudu View Post
    Is there anyway you think we could apply this knowledge toward something, such as figuring a way out to stop cellular senescence Swooping? Thanks for the info, it helps me cope with my hair loss when I learn how something occurs.
    Well preventing or stopping it is easier as you know. If you were to castrate yourself at a early age you would stop the premature senescence problem and basically get yourself rid of AGA. However we know that's not an option. Reversing senescence however is hard. There is many research going into this now, because it is implicated in other diseases too, but also aging for example. Some options that are being explored now is to use some sort of targeted cell destruction technology to get rid of senescent cells. A other option would be to repair them or brute override the signals that mediate the senescence.

    @SogeKing Yes I agree and hopefully the guys get around the culturing problem of dermal papilla cells, that would be a huge step.

    Here is another study which relates to all of this (http://www.papersearch.net/view/deta...l_key=27731029) ;

    Background: Clinical evidence shows that accumulation of 5 α-dihydrotestosterone(DHT) in dermal papilla cells(DPCs) is implicated in androgenetic alopecia. Objectives: To determine whether DHT affects cell growth, cell cycle arrest, cell death, senescence, and induction of reactive oxygen species(ROS), and whether these effects aremediated by microRNA(miRNA)-dependent mechanisms. Methods: We measured cell viability and cell cycle, detected ROS, and performed senescence-associated β-galactosidase assays in normal human DPCs(nHDPCs). Further, we performed miRNA expression profiling using miRNA microarray to determine whether changes in miRNA expression were associated with the cellular effects of DHT. Results: We found that DHT decreased cell growth by inducing cell death and G2 cell cycle arrest and by increasing ROS production and senescence in nHDPCs. 55 miRNAs were up-regulated and 6 miRNAs were down-regulated in DHT-treated nHDPCs. Bioinformatic analysis showed that putative target genes of these up- and down-regulated miRNAs were involved in cell growth, cell cycle arrest, cell death, senescence, and ROS production. Conclusion: These results demonstrate that miRNA expression is altered in DHT-treated nHDPCs and suggest a potential mechanism of DHTinduced cell growth repression, cell cycle arrest, cell death, senescence, and ROS induction.

  5. #15
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    Hey Swooping, this is a great post. I rarely post on this forum, just lurk from time to time, but I think you know your stuff so I guess I can ask you this. I think you mentioned something about it in your post but I didn't quite get it though.

    Question: I've always heard that stress can cause and accelerate hairloss. I've seen some people say it hasn't been proven, but what I wanna know is if it can cause AGA and then if it can accelerate it, or does it only cause something like telogen effluvium (which I think is reversible/temporary)?

    Whenever I see stuff on the internet about stress causing hairloss it's usually articles from stupid magazines that have no scientific facts to back up their claims. Thanks so much for this post!

  6. #16
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    Quote Originally Posted by woodnor View Post
    Hey Swooping, this is a great post. I rarely post on this forum, just lurk from time to time, but I think you know your stuff so I guess I can ask you this. I think you mentioned something about it in your post but I didn't quite get it though.

    Question: I've always heard that stress can cause and accelerate hairloss. I've seen some people say it hasn't been proven, but what I wanna know is if it can cause AGA and then if it can accelerate it, or does it only cause something like telogen effluvium (which I think is reversible/temporary)?

    Whenever I see stuff on the internet about stress causing hairloss it's usually articles from stupid magazines that have no scientific facts to back up their claims. Thanks so much for this post!
    Thanks. Stress can definitely not cause AGA. However indeed AGA ain't the only cause which can bring on hairloss. Outside of that there can be many causes too. Let me give you a theoretical example of stress could possibly bring on hairloss. Stress can cause thyroid problems. We know thyroid problems on itself can cause hairloss. If you look at the literature then;

    http://www.ncbi.nlm.nih.gov/pubmed/25066729
    http://www.ncbi.nlm.nih.gov/pubmed/19825978
    http://www.ncbi.nlm.nih.gov/pubmed/21956127
    http://www.ncbi.nlm.nih.gov/pubmed/20302576

    You can see that thyrotropin releasing hormone and the thyroid have a prominent role in hair follicle cycling too. So if things start to go wrong with your thyroid which can be induced by stress, your hair may suffer too. This is just a example obviously. Stress won't cause AGA though. Hope that helps you. Why by the way are you not sure if you are suffering from AGA?

  7. #17
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    Quote Originally Posted by Swooping View Post
    Thanks. Stress can definitely not cause AGA. However indeed AGA ain't the only cause which can bring on hairloss. Outside of that there can be many causes too. Let me give you a theoretical example of stress could possibly bring on hairloss. Stress can cause thyroid problems. We know thyroid problems on itself can cause hairloss. If you look at the literature then;

    http://www.ncbi.nlm.nih.gov/pubmed/25066729
    http://www.ncbi.nlm.nih.gov/pubmed/19825978
    http://www.ncbi.nlm.nih.gov/pubmed/21956127
    http://www.ncbi.nlm.nih.gov/pubmed/20302576

    You can see that thyrotropin releasing hormone and the thyroid have a prominent role in hair follicle cycling too. So if things start to go wrong with your thyroid which can be induced by stress, your hair may suffer too. This is just a example obviously. Stress won't cause AGA though. Hope that helps you. Why by the way are you not sure if you are suffering from AGA?
    No, I was asking because i wanted to know if my stress ws a contributing factor to my aga. So basically stress can be the root of other problems which cause hair loss, but can this type of hairloss (like the one caused by thyroid problems) be irreversible?
    Thanks for answering by the way

  8. #18
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    Quote Originally Posted by woodnor View Post
    No, I was asking because i wanted to know if my stress ws a contributing factor to my aga. So basically stress can be the root of other problems which cause hair loss, but can this type of hairloss (like the one caused by thyroid problems) be irreversible?
    Thanks for answering by the way
    Well I was just giving an example how stress might contribute to hairloss. A good thing to be sure would to do a blood test and measure the following things; B12, cortisol, Iron, Ferritin, Iodine, TSH. If that is alright then you don't have anything to worry about I think. That is obviously if you don't suffer from alopecia areata or a worse form of alopecia, but if that were the case you would know.

  9. #19
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    Another study which relates to this (on mice though this one);



    Overview of major pathways implicated in AGA in relation to senescence and an overview about how they work in general;


    Senescence-inducing signals, including those that trigger a DNA-damage response (DDR), as well as many other stresses (Fig. 1), usually engage either the p53 or the p16–retinoblastoma protein (pRB) tumour suppressor pathways. Some signals, such as oncogenic RAS, engage both pathways. p53 is negatively regulated by the E3 ubiquitin-protein ligase HDM2 (MDM2 in mice), which facilitates its degradation, and HDM2 is negatively regulated by the alternate-reading-frame protein (ARF). Active p53 establishes the senescence growth arrest in part by inducing the expression of p21, a cyclin-dependent kinase (CDK) inhibitor that, among other activities, suppresses the phosphorylation and, hence, the inactivation of pRB. Senescence signals that engage the p16–pRB pathway generally do so by inducing the expression of p16, another CDK inhibitor that prevents pRB phosphorylation and inactivation. pRB halts cell proliferation by suppressing the activity of E2F, a transcription factor that stimulates the expression of genes that are required for cell-cycle progression. E2F can also curtail proliferation by inducing ARF expression, which engages the p53 pathway. So, there is reciprocal regulation between the p53 and p16–pRB pathways. Interactions among ARF, HDM2, p53, p21, CDKs, pRB and E2F also occur in other cell contexts — for example, during the DDR and reversible or transient growth arrest — so it not yet clear how senescence, as opposed to quiescence or transient growth arrest, is established. It is noteworthy, however, that at least in cell-culture studies, upregulation of p16 is not part of the immediate DDR and does not occur during transient growth arrests or quiescence.

  10. #20
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    So AGA activations varies from age with people depending on when one's DNA get damaged?

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