X-Message-Number: 13260 From: Eugene Leitl <> Date: Tue, 15 Feb 2000 18:56:12 -0800 (PST) Subject: ON THE POSSIBILITIES FOR POSTPONEMENT OF HUMAN AGING ripped from SCIENCE-WEEK February 18, 2000 [...] 6. MEDICAL BIOLOGY: ON THE POSSIBILITIES FOR POSTPONEMENT OF HUMAN AGING Concerning the application of science to the extension of human life span, there are three considerations: a) improved public hygiene and public health measures important in the prevention of disease; b) improved treatment of fatal diseases that appear in middle and old age; c) actual retardation of the biological aging process. With respect to the first two, there has been considerable progress, particularly during the past 100 years; with respect to the third, there has been no real progress at all in terms of results, but our understanding of the biological aging process has significantly improved during the past few decades. ... ... Michael R. Rose (University of California Irvine) presents a review of current ideas concerning the biological aging process, the author making the following points: 1) The author points out that all attempts to restore or sustain youthful vigor in humans have failed to achieve their goal. Individuals who currently survive past 65 years of age are only slightly more likely to enjoy a robust old age than their counterparts 2000 years ago. Although life expectancy has increased during the past century due to advances in medical therapy and sanitation systems, nothing slows the innate processes that cause adults to age and suffer a decline in physiological functioning as they grow older. Successful treatment of one illness late in life often means that another illness takes its place. "Infirmity remains the lot of those older than 80, however much the media may dote on the 90-year old marathon runner." 2) The author states that the current view among evolutionary biologists is that weakened natural selection allows deleterious late-acting genes to spread in a population. Calculations indicate that the force of natural selection on survival in sexually reproducing populations drops soon after the earliest age of reproduction is reached. Aging has evolved because genes that produce deleterious effects late in life meet little or no opposition from natural selection, and thus become rampant in the gene pool. [Editor's note: Contrast with this the approach of molecular biologists evident in the relevant background material below.] 3) In the 1940s and 1950s, J.B.S. Haldane (1892-1964) and P.B. Medawar (1915-1987) were the first to introduce this evolutionary explanation of aging. W.D. Hamilton and B. Charlesworth then made the thesis mathematically rigorous in the 1960s and 1970s. Hamilton and Charlesworth established that for sexually reproducing organisms (i.e., organisms that do not reproduce by splitting in two), the force of natural selection on survival falls with adult age and then disappears entirely late in life. Since natural selection is the source of all adaptation, and thus of health, the hardiness of the population of older organisms declines as natural selection fades out. Eventually, with the continued absence of natural selection at later ages, survival may be so imperiled that optimal conditions and medical care may be unable to keep the older individual alive. 4) Evolutionary theory and some crude experiments suggest that hundreds of genetically determined biochemical pathways influence longevity and might thus be manipulated to postpone aging. So far, however, only a handful of genes that could be involved have been discovered, principally in the unsegmented roundworm (nematode) Caenorhabditis elegans and in the fruit fly Drosophila melanogaster. Whether results in these organisms apply to humans remains to be determined. 5) Among the potential human longevity therapies that have been publicized in recent years are exercise, diet restriction, and delivery of various substances such as growth hormone, the enzyme telomerase, and anti-oxidants. Exercise has not been shown to increase long-term survival; diet restriction has not been studied systematically in humans; increasing hormone levels is potentially dangerous; telomerase experiments have not demonstrated an increase in longevity in any living organism; there is no research demonstrating a longevity-producing anti- oxidant effect in humans, or even research demonstrating a safe method for blocking the production of free radicals or removing free radicals once produced. [Editor's note: There is no direct evidence that the ingestion of so-called "anti-oxidant" foods results in the block or removal of free radicals in human tissues. There is some evidence, however, that the ingestion of certain anti-oxidant substances (e.g., ascorbic acid, vitamin E, beta-carotene) may reduce the risk of human coronary artery disease.] ----------- Michael R. Rose: Can human aging be postponed? (Scientific American December 1999) QY: Michael R. Rose, Univ. of California Irvine, 714-856-6703 ------------------- Summary by SCIENCE-WEEK [http://scienceweek.com] 18Feb00 [For more information: http://scienceweek.com/search/search.htm] ------------------- Related Background: BIOLOGY OF AGING: CALORIC RESTRICTION AND GENE EXPRESSION Most multicellular organisms exhibit a progressive and irreversible physiological decline that characterizes what is called "senescence" -- the aging process. The molecular basis of this process is unknown, but various mechanisms have been postulated, including: a) cumulative damage to DNA leading to genome instability; b) biochemical pathway alterations that lead to changes in *gene expression patterns; c) *telomere shortening in replicative cells; d) oxidative damage to critical macromolecules by reactive oxygen species; and e) nonenzymatic *glycation of proteins. Experimental genetic manipulation of the aging process in multicellular organisms has been achieved in the fruit fly Drosophila through the overexpression of certain enzymes, and in the nematode worm C. elegans through alterations in the *insulin receptor pathway, and in both organisms through the experimental selection of stress-resistant mutants. In mammals, however, the only intervention that appears to slow the intrinsic rate of aging is caloric restriction. Most studies of caloric restriction in mammals have involved laboratory rodents subjected to a long-term 25 to 50 percent reduction in caloric intake without essential nutrient deficiency, and the result in these rodents is a delayed onset of age-associated pathological and physiological changes and an extension of maximum lifespan. Various mechanisms have been postulated to explain this result, including increased DNA repair capacity, altered gene expression, depressed metabolic rate, and reduced oxidative stress. ... ... C-K. Lee et al (4 authors at University of Wisconsin, US) now present a study to examine the molecular events associated with aging in mammals, with experiments involving analysis of the aging process in *skeletal muscle of mice. The authors report that the use of high-density *oligonucleotide arrays representing 6347 genes (5 to 10 percent of the mouse genome) revealed that aging resulted in a differential gene expression pattern indicative of a marked stress response and lower expression of metabolic and biosynthetic genes. Most alterations were either completely or partially prevented by caloric restriction. *Transcriptional patterns of calorie-restricted animals suggest that caloric restriction retards the aging process by causing a metabolic shift toward increased protein turnover and decreased macromolecular damage. The authors state: "The data presented here provide the first global assessment of the aging process in mammals at the molecular level and underscore the utility of large-scale parallel gene expression analysis in the study of complex biological phenomena." ----------- C-K. Lee et al: Gene expression profile of aging and its retardation by caloric restriction. (Science 27 Aug 99 285:1390) QY: Tomas A. Prolla [] ----------- Text Notes: ... ... *gene expression patterns: This refers to the profile of genes in a genome that are actually operating (i.e., undergoing expression) at any point in time. In a mammal, for example, a liver cell is a liver cell because of a particular profile of expressed genes, and what that liver cell is doing at any point in time is determined by variations of that profile. It is the operating patterns (gene expression patterns) of the genome that are the paramount determinants of the behavior of cells. ... ... *telomere: Telomeres are defined ends of chromosomes that contain specific repeated DNA sequences. They are essential for normal chromosome replication, and since their length shortens a bit with each replication, they are believed to be involved in the aging of the cell. ... ... *glycation of proteins: "Glycation" is the post- translational (i.e., after protein synthesis) modification of a protein by the covalent attachment of a sugar residue, the modification resulting from a spontaneous amino-carbonyl reaction ("Maillard reaction"). Glycation of various proteins has recently been implicated in the etiology of various diseases such as the development of Alzheimer's-type pathologies (e.g., dementias). ... ... *insulin receptor pathway: Insulin is a polypeptide chemical messenger (hormone) comprising 51 amino acids in two chains linked by disulphide bridges. The insulin receptor is a specific membrane protein derived from an intracellular precursor and transported from specialized intracellular structures to the cell surface. ... ... *skeletal muscle: In general, the term "skeletal muscle" refers to striated muscle fibers (singly or in a collection) attached at one or both ends of a part of the body skeleton. "Striated muscle" is muscle usually associated with voluntary motion, the adjective "striated" arising from the microscopically visible cross striations which occur in the fibers as a result of regular overlapping of thick and thin muscle fiber filaments (myofilaments). In general, such fibers are specialized for rapid contraction and relaxation. ... ... *oligonucleotide arrays: The essential idea concerning the use of "arrays" in determining gene expression patterns involves the fact that for every gene (DNA sequence) undergoing expression there exists in the cytoplasm a specific RNA whose nucleotide sequence is a result of transcription of that gene (see next note on "transcriptional patterns"). There exists now a technique for profiling the large variety of RNAs that can be extracted from tissue, the technique depending on highly ordered arrays of large numbers of oligonucleotide probes (essentially pieces of DNA) in a parallel format, with specific DNA-RNA interactions producing localized fluorescences, and the array of fluorescences providing a profile of detectable RNAs. A determination of the profile of existing RNA sequences implies the profile of the DNA sequences (genes) that are being naturally expressed in the genome, and if one knows which genes are involved with which functions in that particular cell or organism, one has obtained a profile of existing functions. The use of such arrays of nucleotide probes (sometimes called micro- arrays or "chips") is now highly automated ("robotic"), and the technique can be used to determine the expression profile of thousands of genes in an ensemble of cells. ... ... *Transcriptional patterns: "Transcription" is the process by which genetic information in DNA is converted into RNA. ------------------- Summary & Notes by SCIENCE-WEEK [http://scienceweek.com] 24Sep99 ------------------- Related Background: AGING, LIFESPAN, AND SENESCENCE Our knowledge of the basis of senescence of cells, tissues, and organisms (including humans) has entered a new phase in recent decades because of the new vistas opened by molecular biology. Model systems have started to provide insights, and one important approach has been the identification of genes that determine the lifespan of an organism. The very existence of genes that when mutated can extend lifespan suggests to many researchers that one or a few processes may be critical in aging, and that a slowing of these processes may slow aging itself. ... ... In a short review of current research in the molecular biology of aging and lifespan, L. Guarente et al make the following points: 1) In the budding yeast Saccharomyces cerevisiae, aging results from the asymmetry of cell division, which produces a large mother cell and a small daughter cell arising from the bud. Much of the macromolecular composition of the daughter cell is newly synthesized, whereas the composition of the mother cell grows older with each cell division. It has been shown that mother cells of this yeast species divide a relatively fixed number of times, and exhibit a slowing of the cell cycle, cell enlargement, and sterility. Analysis of *ribosomal DNA in old cells reveals an accumulation of *extrachromosomal ribosomal DNA of discrete sizes, apparently representing a cumulative fragmentation of chromosomal ribosomal DNA. The authors suggest it will be of great interest to assess the generality of this process as an aging mechanism. 2) In *Caenorhabditis elegans (a *nematode worm; see notes), the *neurosecretory system regulates whether animals enter the reproductive life cycle or arrest development at a primitive *diapause stage. Developmental arrest is apparently induced by a *pheromone and involves behavioral and morphological changes in many tissues of the animal, with the lifespan becoming 4 to 8 times longer than that of the normal 3-week lifespan of fully developed animals. Declines in pheromone concentration induce recovery to reproductive adults with normal metabolism and lifespan. Genes that regulate the function of the C. elegans diapause and the neuroendocrine aging pathway have been identified, and at least one of these genes codes for an *insulin-like receptor apparently involved in metabolism. The authors suggest that if the association of longevity and diapause is general, it is possible that *polymorphisms in the human insulin receptor-signaling pathway genes and related gene *homologues may underlie genetic variation in human longevity. 3) In plants, there is a large range of lifespans in the various plant kingdoms. Certain tree species live for well over a century, whereas other plants complete their life cycle in a few weeks. The "yellowing" of leaves is often referred to in the plant literature as leaf senescence or the "senescence syndrome" -- referring to the process by which nutrients are mobilized from the dying leaf to other parts of the plant to support their growth. The senescence syndrome is characterized by distinct cellular and molecular changes, with the chloroplast the first part of the cell to undergo disassembly (producing the "yellowing"). In many plant species, certain hormones can either enhance or delay senescence. Although the genes that are expressed during the plant senescence syndrome (as well as ways to manipulate such senescence) have been identified, much remains to be done to understand the molecular basis of aging in plants. For example, nothing is known about the signal transduction pathways that lead to altered gene expression during senescence, or how plant hormones such as *cytokinin influence senescence. But there are now many tools to explore this process. The authors conclude: "It remains to be seen whether common mechanisms link the aging process in diverse organisms." ----------- L. Guarente et al (3 authors at 3 installations, US) Aging, lifespan, and senescence. (Proc. Natl. Acad. Sci. US 15 Sep 98 95:11034) QY: Leonard Guarente, Mass. Inst. of Technology 617-253-1000. ----------- Text Notes: ... ... *ribosomal DNA: A ribosome (not to be confused with riboZYME) is a small particle, a complex of various ribonucleic acid component subunits and proteins that functions as the site of protein synthesis. The term "ribosomal DNA" refers to the gene or genes that code for the RNA in ribosomes. In other words, the term "ribosomal DNA" does not refer to any DNA in ribosomes (there is no DNA in ribosomes). ... ... *extrachromosomal: In general, this refers to anything outside of chromosomes, and in this case to DNA fragments unincorporated into chromosomal DNA. ... ... *Caenorhabditis elegans: This is a small (1 mm) nematode worm. It is transparent, hermaphroditic, free-living, and found in soil. It has a relatively small genome (approximately 19,000 genes), and only a few types of cells in its body. It has a 16-hr embryogenesis that can be achieved in a petri dish, and is thus highly suitable for the study of developmental and behavioral genetics. ... ... *nematode: An abundant and ubiquitous phylum of unsegmented roundworms. ... ... *neurosecretory system: In general, all neural systems contain both neurons that themselves secrete chemical messengers and neurons that signal special secretory cells to secrete chemical messengers. A neurosecretory pathway is a delineated signaling system that involves such a resultant secretion. ... ... *diapause: In general, this refers to any programmed period of suspended development in invertebrates. ... ... *pheromone: In general, a chemical substance which, when released into an animal's surroundings, influences the development or behavior of other individuals of the same species. ... ... *insulin: A protein hormone that promotes uptake by body cells of free glucose and/or amino acids, depending on target cell type. ... ... *polymorphisms: A genetic polymorphism is a naturally occurring variation in the normal nucleotide sequence of the genome within individuals in a population. Variations are denoted as polymorphisms only if they cannot be accounted for by recurrent mutation and occur with a frequency of at least about 1 percent. ... ... *homologues: In general, the term "homologous" means having the same structure. But the term has special uses in genetics and evolution biology. ... ... *cytokinin: A group of plant growth substances. They are chemically identified as derivatives of the purine base adenine. They stimulate cell division and determine the course of differentiation. They work synergistically with other plant hormones called "auxins". ------------------- Summary & Notes by SCIENCE-WEEK [http://scienceweek.com] 6Nov98 [...] Rate This Message: http://www.cryonet.org/cgi-bin/rate.cgi?msg=13260