age-1(hx546) is a recessive mutant allele in Caenorhabditis elegans that results in an increase in mean life span averaging 40% and in maximal life span averaging 60% at 20 degrees; at 25 degrees age-1(hx546) averages a 65% increase in mean life span (25.3 days vs. 15.0 days) and a 110% increase in maximum life span (46.2 days vs. 22.0 days for wild-type hermaphrodites). Mutant males also show extended life spans. age-1(hx546) is associated with a 75% decrease in hermaphrodite self-fertility as compared to the age-1+ allele at 20 degrees. Using two novel strategies for following the segregation of age-1, we present evidence that longer life results from a mutation in a single gene that increases the probability of survival at all chronological ages. The long-life and reduced-fertility phenotypes cosegregate and are tightly linked to fer-15, a locus on linkage group II. age-1(hx546) does not affect the timing of larval molts, the length of embryogenesis, food uptake, movement, or behavior in any way tested. Although age-1(hx546) lowers hermaphrodite self-fertility, it does not markedly affect the length of the reproductive period with all the increase in life expectancy due to an increase in the length of postreproductive life. In so far as we are aware, this mutant in age-1 is the only instance of a well-characterized genetic locus in which the mutant form results in lengthened fife. It is likely that the action of age-1 in lengthening life results not from eliminating a programmed aging function but rather from reduced hermaphrodite self-fertility or from some other unknown metabolic or physiologic alteration.

https://www.genetics.org/content/genetics/118/1/75.full.pdf

A mutation in the age-1 gene in Caenorhabditis elegans lengthens life and reduces hermaphrodite fertility.

Neural bases of visual deficits during aging.

Little is known about the importance of genetic effects on individual differences in cognitive abilities late in life. We present the first report from the Swedish Adoption/Twin Study of Aging (SATSA) for cognitive data, including general cognitive ability and 13 tests of specific cognitive abilities. The adoption/twin design consists of identical twins separated at an early age and reared apart (46 pairs), identical twins reared together (67 pairs), fraternal twins reared apart (100 pairs), and fraternal twins reared together (89 pairs); average age was 65 years. Heritability of general cognitive ability in these twins was much higher (about 80%) than estimates typically found earlier in life (about 50%). Consistent with the literature, heritabilities of specific cognitive abilities were lower than the heritability of general cognitive ability but nonetheless substantial. Average heritabilities for verbal, spatial, perceptual speed, and memory tests were, respectively, 58%, 46%, 58%, and 38%.

/pdf/a-quantitative-genetic-analysis-of-cognitive-abilities-5e0ipggzmd.pdf

A Quantitative Genetic Analysis of Cognitive Abilities During the Second Half of the Life Span

1. Differences in the effect of age on structure-function relationships of limb muscles of mdx (dystrophin null) and control mice have not been resolved. We tested the hypotheses that, compared with limb muscles from age-matched control mice, limb muscles of 6- to 17-month-old mdx mice are larger but weaker, with lower normalised force and power, whereas those from 24- to 28-month-old mdx mice are smaller and weaker. 2. The maximum isometric tetanic force (P(o)) and power output of limb muscles from 6-, 17-, 24- and 28-month-old mdx and control mice were measured in vitro at 25 degrees C and normalised with respect to cross-sectional area and muscle mass, respectively. 3. Body mass at 6 and 28 months was not significantly different in mdx and control mice, but that of control mice increased 16 % by 17 months and then declined 32 % by 28 months. The body masses of mdx mice declined linearly with age with a decrease of 25 % by 28 months. From 6 to 28 months of age, the range in the decline in the masses of EDL and soleus muscles of mdx and control mice was from 16 to 28 %. The muscle masses of mdx mice ranged from 9 % to 42 % greater than those of control mice at each of the four ages and, even at 28 months, the masses of EDL and soleus muscles of mdx mice were 17 % and 22 % greater than control values. 4. For mdx mice of all ages, muscle hypertrophy was highly effective in the maintenance of control values for absolute force for both EDL and soleus muscles and for absolute power of soleus muscles. Throughout their lifespan, muscles of mdx mice displayed significant weakness with values for specific P(o) and normalised power approximately 20 % lower than values for control mice at each age. For muscles of both strains, normalised force and power decreased approximately 28 % with age, and consequently weakness was more severe in muscles of old mdx than in those of old control mice.

/pdf/force-and-power-output-of-fast-and-slow-skeletal-muscles-279cuatr8p.pdf

Force and power output of fast and slow skeletal muscles from mdx mice 6‐28 months old

Oxygen free radicals, any chemical moiety containing an oxygen atom with an unpaired electron in the outer orbital shell, are generated during many normal biochemical reactions in living tissue. The unpaired electron makes these compounds highly reactive and they can initiate disruptive peroxidation reactions with various substrates important to the survival of cells such as proteins, lipids and nucleic acids. A fairly complex defense system has evolved to protect living tissue from free radicals and to minimize the damage they might cause. Neurons are especially vulnerable to free radical attack and impaired defenses or exposure to excess free radicals can lead to neuronal death. Free radicals contribute to neuronal loss in cerebral ischemia and hemorrhage and may be involved in the degeneration of neurons in epilepsy, schizophrenia, tardive dyskinesia, normal aging, Parkinson's Disease and Alzheimer's Disease. The development of drugs that limit or prevent the attack of free radicals on neurons would be...

Oxygen free radicals and brain dysfunction.

From 1964 to 1972, Academic Press Inc published a series of books entitled Advances in Gerontological Research , edited by Bernard Strehler, which periodically reviewed the progress in biomedical gerontology. Unfortunately, in the intervening decade, there have not been any series of books of a similar nature that unfailingly updated each area of biologic research in aging every year or two. Other gerontologically related series such as Raven's Aging series, Karger's Interdisciplinary Topics in Gerontology , and Liss' own Modern Aging Research series, are published at irregular intervals, and are generally very narrow in scope (usually consisting of proceedings of various highly specialized symposia, of little interest to those not specializing in the subject). Review of Biological Research in Aging , volume 1, admirably fills this gap, and it is hoped that further volumes in this planned series will materialize. This first volume has set a precedent for excellence, which, if emulated by

Review of Biological Research in Aging

To the Editor.— Regarding the article "Losing Weight Through Exercise" (1980;244:377), in the authors' disparagement of "effortless weight reduction" by methods that cause increased water loss, they make the often repeated misleading statement that "body weight may be temporarily reduced until rehydration occurs." This implies that there is no caloric consumption involved in the water loss. The same statement could be made for the weight loss incurred by a marathon runner during a race and his subsequent "weight gain" after rehydration. The fact overlooked by most people who attempt to debunk saunas and other devices that cause enhanced sweating is that the water does not just "leak out" of the body. Sweating is a part of the complex thermoregulatory process of the body involving substantial increases in heart rate, cardiac output, 1,2 and metabolic rate, 3-4 and consumes considerable energy. In a sauna, heat is absorbed by the subject from

Effect of Sweating

In Reply.— While I do not have any data on the caloric intake of persons living in tropical zones, Guyton1points out that the basal metabolic rate of those living in tropical zones is substantially less than that of those living in colder climates, owing in part to decreased thyroxine secretion. The effects of a sauna can probably be much better determined by studying persons exposed to a sauna, rather than comparing the caloric consumption of persons residing in different climatological zones. Using whole-body gradient calorimetry Benzinger2found that a dramatic increase in metabolic rate occurred as the core temperature was increased. Also, Kleiber3shows that at temperatures greater than 37 °C, there is a steep increase in metabolic rate. In a study to determine the effectiveness of a sauna as a conditioning device, Pribil and Matousek4found that after seven weeks of only two sauna

Effects of the Sauna-Reply

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Review of Biological Research in Aging

Effect of Sweating

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