{"id":462,"date":"2016-01-29T15:15:48","date_gmt":"2016-01-29T15:15:48","guid":{"rendered":"http:\/\/joshmitteldorf.peachpuff-wolverine-566518.hostingersite.com\/?p=462"},"modified":"2016-01-29T15:15:48","modified_gmt":"2016-01-29T15:15:48","slug":"is-aging-controlled-from-the-brain-npy-and-alk5","status":"publish","type":"post","link":"https:\/\/scienceblog.com\/joshmitteldorf\/2016\/01\/29\/is-aging-controlled-from-the-brain-npy-and-alk5\/","title":{"rendered":"Is Aging Controlled from the Brain?  NPY and ALK5"},"content":{"rendered":"<p><i><span style=\"font-weight: 400\">For more than a decade, <\/span><\/i><a href=\"https:\/\/www.researchgate.net\/profile\/Claudia_Cavadas2\/publications\"><i><span style=\"font-weight: 400\">Claudia Cavadas<\/span><\/i><\/a><i><span style=\"font-weight: 400\"> of the Center for Neuroscience in Coimbra, Portugal has been on the trail of a signal molecule that comes from a region of the brain associated with timing. \u00a0It\u2019s a small protein called Neuropeptide Y, and Cavadas has recently collected the body of evidence that it is a central determinant of aging in the brain and throughout the body. \u00a0Whether or not NPY proves to be the Philosopher\u2019s Stone, I think she\u2019s on the right track to be investigating neuroendocrine origins of aging.<\/span><\/i><\/p>\n<p><em>The present\u00a0column\u00a0also contains a (belated) update on ALK5 and TGF<\/em>\u03b2<em>.<\/em><\/p>\n<hr \/>\n<p><span style=\"font-weight: 400\">Since the genetic science of aging began to take off in the 1990s, the biggest surprise has been the extent to which aging is centrally orchestrated. \u201dRegulated\u201d is the accepted word, but I don\u2019t hesitate to say \u201cprogrammed\u201d. \u00a0For those of us interested in intervening to slow or reverse the process, the burning question is: how is the program implemented? \u00a0If the process is centrally orchestrated, where is the orchestra\u2019s conductor? \u00a0<\/span><\/p>\n<p>We have the same genes when we are old as when we are young, but different genes are turned on and off in different stages of life. \u00a0How genes are turned on and off is the science of <i><span style=\"font-weight: 400\">epigenetics<\/span><\/i><span style=\"font-weight: 400\">,<\/span> <span style=\"font-weight: 400\">and we are just beginning to untangle the set of chemical add-ons that bind to the chromosome or to the <\/span><i><span style=\"font-weight: 400\">histones<\/span><\/i><span style=\"font-weight: 400\">, protein spindles around which the chromosome is spooled. \u00a0Chemical signals that turn whole suites of genes on and off are called <\/span><i><span style=\"font-weight: 400\">transcription factors<\/span><\/i><span style=\"font-weight: 400\">, and these can be big molecules or small, proteins or RNAs, very specific and targeted to a single gene, or aimed more generally at large swaths of the chromosome. <\/span><\/p>\n<p>At the least, transcription factors are able to regulate the body\u2019s rate of aging. \u00a0But I see evidence that the chemical signals have even more power\u2014the chemical signals tell the body how old it is. \u00a0Change the signals, and the body can change its age.<\/p>\n<p><span style=\"font-weight: 400\">When we think this way, the questions \u201cwhat are these signals?\u201d and \u201cwhere do they come from?\u201d become exciting and highly charged. \u00a0The most intuitive and logical place to look for a source of age signals is in the brain. \u00a0Here are four reasons to look to the brain\u2019s hormone center, the <\/span><i><span style=\"font-weight: 400\">neuroendocrine region<\/span><\/i><span style=\"font-weight: 400\">, as a source of aging signals.<\/span><\/p>\n<ul>\n<li style=\"font-weight: 400\"><span style=\"font-weight: 400\">We know that aging is highly plastic and adaptive depending on behavior and environment. \u00a0To sense many factors and make a decision about aging, it seems that the combined forces of the nerves and endocrine signal transducers in the brain are best equipped for the job.<\/span><\/li>\n<li style=\"font-weight: 400\"><span style=\"font-weight: 400\">The <\/span><i><span style=\"font-weight: 400\">hypothalamus<\/span><\/i><span style=\"font-weight: 400\"> is a neuroendocrine region of the brain already known to house the seat of the 24-hour clock that synchronizes our circadian rhythms, the <\/span><i><span style=\"font-weight: 400\">suprachiasmatic nucleus<\/span><\/i><span style=\"font-weight: 400\">. \u00a0<\/span><\/li>\n<li style=\"font-weight: 400\"><span style=\"font-weight: 400\">The hypothalamus is also responsible for flooding the body with at least one of the <\/span><i><span style=\"font-weight: 400\">transcription factors <\/span><\/i><span style=\"font-weight: 400\">that increase destructive inflammation late in life (<\/span><a href=\"http:\/\/www.nature.com\/nature\/journal\/v497\/n7448\/abs\/nature12143.html\"><span style=\"font-weight: 400\">NFkB<\/span><\/a><span style=\"font-weight: 400\">).<\/span><\/li>\n<li style=\"font-weight: 400\"><span style=\"font-weight: 400\">In a worm experiment fifteen years ago, genes for aging were modified in different systems of the worm, and the modifications were effective in changing the worm life span only when the genes were modified in the nervous system (not in skin or muscle or digestive system).<\/span><\/li>\n<\/ul>\n<p><span style=\"font-weight: 400\">This mode of thinking suggests that Cavadas has been digging at the taproot of aging, and that the signal she has identified may be of central importance. \u00a0In a <\/span><a href=\"http:\/\/www.sciencedirect.com\/science\/article\/pii\/S0166223615002076\"><span style=\"font-weight: 400\">recent paper<\/span><\/a><span style=\"font-weight: 400\">, Cavadas lays out the case for a central role in Neuropeptide Y in dictating the age of the body. \u00a0<\/span><\/p>\n<blockquote><p>Accumulating evidence suggests that neuropeptide Y (NPY) has a role in aging and lifespan determination. In this review, we critically discuss age-related changes in NPY levels in the brain, together with recent findings concerning the contribution of NPY to, and impact on, six hallmarks of aging, specifically:<\/p>\n<ul>\n<li>loss of proteostasis<\/li>\n<li>stem cell exhaustion<\/li>\n<li>altered intercellular communication<\/li>\n<li>deregulated nutrient sensing<\/li>\n<li>cellular senescence, and<\/li>\n<li>mitochondrial dysfunction<\/li>\n<\/ul>\n<\/blockquote>\n<p>NPY is a small protein, with 36 amino acids, found in the nervous systems of all higher animals. \u00a0It is one of the most abundant neuroendocrine proteins, but since these chemicals are very powerful signal molecules, the body\u2019s total inventory is measured in \u03bcg (millionths of a gram). \u00a0NPY has various roles related to appetite, anxiety, memory, and circadian rhythm. \u00a0Levels of NPY decline with age, especially in certain regions of the brain. \u00a0Caloric Restriction also elevates levels of NPY. \u00a0High blood sugar levels tend to inhibit NPY. \u00a0And there is a bit of evidence that NPY is necessary for CR to extend life span: \u00a0Mice in which the NPY gene has been knocked out <a href=\"http:\/\/www.nature.com\/articles\/srep04517\"><span style=\"font-weight: 400\">don\u2019t respond to CR<\/span><\/a><span style=\"font-weight: 400\">. NPY is also associated with cancer suppression in mice.<\/span><\/p>\n<p><i><span style=\"font-weight: 400\">Autophagy<\/span><\/i><span style=\"font-weight: 400\"> is the process by which cells break down and recycles damaged molecules. \u00a0As we age, autophagy slows down and damaged molecules accumulate: \u00a0misfolded proteins, cross-linked sugars, lipofuscin and amyloids. \u00a0A central function of NPY is in <a href=\"http:\/\/www.tandfonline.com\/doi\/abs\/10.1080\/15548627.2015.1062202\" target=\"_blank\">promoting autophagy<\/a>, especially in the brain. \u00a0<\/span><\/p>\n<p><span style=\"font-weight: 400\">The NPY gene can be read in a way that transcribes only the second half, and the result is a protein that binds to mitochondria and improves energy efficiency, reduces ROS damage. \u00a0Some studies suggest that NPY can extend the useful life of stem cells, and delay cellular senescence. \u00a0Links to anti-inflammatory chemistry are less well established.<\/span><\/p>\n<p>&nbsp;<\/p>\n<p><b>Why NPY probably is not the Philosopher\u2019s Stone<\/b><\/p>\n<p><span style=\"font-weight: 400\">All this suggests a role for NPY in aging, and the possibility that increasing NPY might increase life span. \u00a0But it is not easy to increase the body\u2019s transcription of a target protein. \u00a0(It is easier to block a protein that is bad than to promote one that is good.) \u00a0And my guess is that we will find signals further upstream from NPY that are even more effective points of intervention. \u00a0The guess is based on the fact that NPY is a neurotransmitter, an \u201cend-use\u201d molecule. \u00a0I suspect that the upstream source of aging will be found in transcription factors, the molecules that bind to DNA and determine which genes are expressed.<\/span><\/p>\n<p>&nbsp;<\/p>\n<p><b>Other Signal Molecules from the Brain<\/b><\/p>\n<p><span style=\"font-weight: 400\">TGF\u03b2 might be a good candidat for the first brain signal to become a target for anti-aging therapy. TGF\u03b2 is a not a transcription factor but a cytokine, a signal protein that affects the energy metabolism and, in particular, inflammatory response. \u00a0It comes not from the hypothalamus, but from the hippocampus, another part of the brain, an inch or two underneath. \u00a0TGF\u03b2 works against us, i.e., we produce more and more of it as we age, and it rallies the inflammatory legions that promote arterial diseases and cancer. \u00a0We would want to block its action, and that might not be too difficult.<\/span><\/p>\n<p><span style=\"font-weight: 400\">One of the targets, receptors into which the TGF\u03b2 molecule plugs to do its work, is called <\/span><a href=\"http:\/\/hplusmagazine.com\/2015\/05\/21\/breakthrough-paper-alk5-inhibitor-a-single-drug-simultaneously-rejuvenates-hippocampal-neurogenesis-and-myogenesis-in-the-same-old-mammal\/\"><span style=\"font-weight: 400\">ALK5<\/span><\/a><span style=\"font-weight: 400\">. \u00a0Jamming ALK5 has been promoted by the <\/span><a href=\"http:\/\/vcresearch.berkeley.edu\/faculty\/irina-conboy\"><span style=\"font-weight: 400\">Conboy lab at Berkeley<\/span><\/a><span style=\"font-weight: 400\"> and others as a strategy to test further. \u00a0ALK5 inhibitor can be injected deep into the body cavity, where it has already been shown to promote new growth in both muscles and nerves in mice. \u00a0This function is apparently related to its role as antagonist to TGF\u03b2. \u00a0Remarkably, stem cells retain their ability to regenerate new tissue well into old age, but they receive signals telling them to stand down. \u00a0Simply changing the signaling environment can make an old stem cell act young. \u00a0This has been a major theme of the Conboys\u2019 work.<\/span><\/p>\n<p><span style=\"font-weight: 400\">What good is TGF\u03b2? \u00a0The story is complicated. \u00a0The molecule can apparently be <\/span><a href=\"http:\/\/www.sciencedirect.com\/science\/article\/pii\/S1471489209000502\"><span style=\"font-weight: 400\">pro-inflammatory or anti-inflammatory<\/span><\/a><span style=\"font-weight: 400\">, also <\/span><a href=\"http:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3512574\/\"><span style=\"font-weight: 400\">pro-cancer or anti-cancer<\/span><\/a><span style=\"font-weight: 400\">. \u00a0This relates to the <\/span><a href=\"https:\/\/scienceblog.com\/joshmitteldorf\/2015\/08\/07\/the-mystery-of-aging-solved-at-last\/\"><span style=\"font-weight: 400\">GDF11 controversy<\/span><\/a><span style=\"font-weight: 400\">, too. \u00a0GDF11 is in the TGF\u03b2 family. \u00a0To me, the Conboys are a trusted source, and they have systematically built a case that too much TGF\u03b2 in later life is a big factor leading to more inflammation and less stem cell activity.<\/span><\/p>\n<p><span style=\"font-weight: 400\">Their ALK5 inhibitor has only been tested for short-term benefits. \u00a0The next step is to do life span studies in mice with ALK5 inhibitor.<\/span><\/p>\n<p>&nbsp;<\/p>\n","protected":false},"excerpt":{"rendered":"<p>For more than a decade, Claudia Cavadas of the Center for Neuroscience in Coimbra, Portugal has been on the trail of a signal molecule that comes from a region of the brain associated with timing. \u00a0It\u2019s a small protein called Neuropeptide Y, and Cavadas has recently collected the body of evidence that it is a &#8230; <a title=\"Is Aging Controlled from the Brain?  NPY and ALK5\" class=\"read-more\" href=\"https:\/\/scienceblog.com\/joshmitteldorf\/2016\/01\/29\/is-aging-controlled-from-the-brain-npy-and-alk5\/\" aria-label=\"Read more about Is Aging Controlled from the Brain?  NPY and ALK5\">Read more<\/a><\/p>\n","protected":false},"author":65,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"jetpack_post_was_ever_published":false,"_jetpack_newsletter_access":"","_jetpack_dont_email_post_to_subs":false,"_jetpack_newsletter_tier_id":0,"_jetpack_memberships_contains_paywalled_content":false,"_jetpack_memberships_contains_paid_content":false,"footnotes":""},"categories":[1],"tags":[],"class_list":["post-462","post","type-post","status-publish","format-standard","hentry","category-uncategorized"],"yoast_head":"<!-- This site is optimized with the Yoast SEO Premium plugin v27.4 (Yoast SEO v27.4) - https:\/\/yoast.com\/product\/yoast-seo-premium-wordpress\/ -->\n<title>Is Aging Controlled from the Brain? NPY and ALK5 - Josh Mitteldorf<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/scienceblog.com\/joshmitteldorf\/2016\/01\/29\/is-aging-controlled-from-the-brain-npy-and-alk5\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Is Aging Controlled from the Brain? NPY and ALK5\" \/>\n<meta property=\"og:description\" content=\"For more than a decade, Claudia Cavadas of the Center for Neuroscience in Coimbra, Portugal has been on the trail of a signal molecule that comes from a region of the brain associated with timing. \u00a0It\u2019s a small protein called Neuropeptide Y, and Cavadas has recently collected the body of evidence that it is a ... 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The surprising fact that our bodies are genetically programmed to age and to die offers an enormous opportunity for medical intervention. It may be that therapies to slow the progress of aging need not repair or regenerate anything, but only need to interfere with an existing program of self-destruction. Mitteldorf has taught a weekly yoga class for thirty years. He is an advocate for vigorous self care, including exercise, meditation and caloric restriction. After earning a PhD in astrophysicist, Mitteldorf moved to evolutionary biology as a primary field in 1996. He has taught at Harvard, Berkeley, Bryn Mawr, LaSalle and Temple University. He is presently affiliated with MIT as a visiting scholar. In private life, Mitteldorf is an advocate for election integrity as well as public health. He is an avid amateur musician, playing piano in chamber groups, French horn in community orchestras. His two daughters are among the first children adopted from China in the mid-1980s. Much to the surprise of evolutionary biologists, genetic experiments indicate that aging has been selected as an adaptation for its own sake. This poses a conundrum: the impact of aging on individual fitness is wholly negative, so aging must be regarded as a kind of evolutionary altruism. Unlike other forms of evolutionary altruism, aging offers benefits to the community that are weak, and not well focussed on near kin of the altruist. This makes the mechanism challenging to understand and to model. more at http:\\\/\\\/mathforum.org\\\/~josh\",\"sameAs\":[\"http:\\\/\\\/AgingAdvice.org\"],\"url\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/author\\\/joshmitteldorf\\\/\"}]}<\/script>\n<!-- \/ Yoast SEO Premium plugin. -->","yoast_head_json":{"title":"Is Aging Controlled from the Brain? 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NPY and ALK5"}]},{"@type":"WebSite","@id":"https:\/\/scienceblog.com\/joshmitteldorf\/#website","url":"https:\/\/scienceblog.com\/joshmitteldorf\/","name":"Josh Mitteldorf","description":"Aging Matters","publisher":{"@id":"https:\/\/scienceblog.com\/joshmitteldorf\/#organization"},"potentialAction":[{"@type":"SearchAction","target":{"@type":"EntryPoint","urlTemplate":"https:\/\/scienceblog.com\/joshmitteldorf\/?s={search_term_string}"},"query-input":{"@type":"PropertyValueSpecification","valueRequired":true,"valueName":"search_term_string"}}],"inLanguage":"en-US"},{"@type":"Organization","@id":"https:\/\/scienceblog.com\/joshmitteldorf\/#organization","name":"Josh Mitteldorf","url":"https:\/\/scienceblog.com\/joshmitteldorf\/","logo":{"@type":"ImageObject","inLanguage":"en-US","@id":"https:\/\/scienceblog.com\/joshmitteldorf\/#\/schema\/logo\/image\/","url":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-content\/uploads\/sites\/2\/2024\/09\/1058476001.jpg","contentUrl":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-content\/uploads\/sites\/2\/2024\/09\/1058476001.jpg","width":864,"height":363,"caption":"Josh Mitteldorf"},"image":{"@id":"https:\/\/scienceblog.com\/joshmitteldorf\/#\/schema\/logo\/image\/"}},{"@type":"Person","@id":"https:\/\/scienceblog.com\/joshmitteldorf\/#\/schema\/person\/214c5d1dad9f15c48f03128d5cfccdb1","name":"Josh Mitteldorf","image":{"@type":"ImageObject","inLanguage":"en-US","@id":"https:\/\/secure.gravatar.com\/avatar\/d3a8498f3d727156673030716d233edc57840f110d501b1b523e1780e9043b92?s=96&d=mm&r=g","url":"https:\/\/secure.gravatar.com\/avatar\/d3a8498f3d727156673030716d233edc57840f110d501b1b523e1780e9043b92?s=96&d=mm&r=g","contentUrl":"https:\/\/secure.gravatar.com\/avatar\/d3a8498f3d727156673030716d233edc57840f110d501b1b523e1780e9043b92?s=96&d=mm&r=g","caption":"Josh Mitteldorf"},"description":"Josh Mitteldorf studies evolutionary theory of aging using computer simulations. The surprising fact that our bodies are genetically programmed to age and to die offers an enormous opportunity for medical intervention. It may be that therapies to slow the progress of aging need not repair or regenerate anything, but only need to interfere with an existing program of self-destruction. Mitteldorf has taught a weekly yoga class for thirty years. He is an advocate for vigorous self care, including exercise, meditation and caloric restriction. After earning a PhD in astrophysicist, Mitteldorf moved to evolutionary biology as a primary field in 1996. He has taught at Harvard, Berkeley, Bryn Mawr, LaSalle and Temple University. He is presently affiliated with MIT as a visiting scholar. In private life, Mitteldorf is an advocate for election integrity as well as public health. He is an avid amateur musician, playing piano in chamber groups, French horn in community orchestras. His two daughters are among the first children adopted from China in the mid-1980s. Much to the surprise of evolutionary biologists, genetic experiments indicate that aging has been selected as an adaptation for its own sake. This poses a conundrum: the impact of aging on individual fitness is wholly negative, so aging must be regarded as a kind of evolutionary altruism. Unlike other forms of evolutionary altruism, aging offers benefits to the community that are weak, and not well focussed on near kin of the altruist. This makes the mechanism challenging to understand and to model. more at http:\/\/mathforum.org\/~josh","sameAs":["http:\/\/AgingAdvice.org"],"url":"https:\/\/scienceblog.com\/joshmitteldorf\/author\/joshmitteldorf\/"}]}},"jetpack_featured_media_url":"","jetpack_shortlink":"https:\/\/wp.me\/pgtN8h-7s","jetpack_sharing_enabled":true,"_links":{"self":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/posts\/462","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/users\/65"}],"replies":[{"embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/comments?post=462"}],"version-history":[{"count":0,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/posts\/462\/revisions"}],"wp:attachment":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/media?parent=462"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/categories?post=462"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/tags?post=462"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}