Nature Precedings - Tag feed for Aging

Aging as a consequence of misrepair—A novel theory of aging

Thomas Michelitsch — Wed, 17 Jun 2009 20:08:26 UTC

It is now increasingly realized that the underlying mechanisms which govern aging is a complex interplay of genetic regulation and damage accumulation. Aging as a result of accumulation of ‘faults’ on cellular and molecular levels, has been proposed in the damage (fault)-accumulation theory by Kirkwood 2006. However, this theory fails to explain some aging phenotypes such as fibrosis and premature aging, since terms such as ‘damage’ and ‘fault’ are not specified. Therefore we introduce here a specification of the underlying mechanism of aging and arrive at a novel theory: aging of the body is a result of the accumulation of Misrepair of tissue. It emphasizes: a) it is Misrepair, not the original damage, that accumulates and leads to aging; and b) aging can occur at different levels, however aging of the body takes place at least on the tissue level, but not necessarily on cellular/molecular level. The novel concept of Misrepair introduced here unifies the understanding of the roles of environmental damage, repair, gene regulation, and multicellular structure in the aging process. The Misrepair-accumulation theory introduced in the present paper gives explanations for the aging phenotypes, premature aging, and the difference of longevity in different species, and is consistent with the point of view of physical theory of complex adaptive systems.

MIF-AMPK cascades

Ji Li — Fri, 12 Jun 2009 14:49:13 UTC

Withdrawn for publication

First Hematological Signals of Latent Anemia to Aging Population

Aurelian Udristioiu — Tue, 26 May 2009 10:52:57 UTC

Anemia is an independent risk factor for morbidity and mortality in an array of disorders common to seniors including cancer, renal diseases and heart diseases. The aim of this study was to identify the first hematological signals of latent anemia to aging population using as screening the hematological aspects of cells from peripheral blood and additional tests, establishing the etiology of anemia in the elderly.Method: Additional to level of hemoglobin(HGB) and hematocrit (HCT) have been included Hematological Indexes( MCV, HCV, MCHC ), red cell distribution width,(RDW), reticulocyte count (RET), serum iron (SI), total iron binding capacity,(TIBC), transferrin saturation index, (TSI), serum ferritin( SF), on an study of 140 adult hospitalized patients, in wars with chronic diseases males and females with ages past 65 years.Results: Anemia of chronic diseases (ACD) is more common in the elderly than other group.In ACD correlation of hematological testes was following: 32 % with normal HGB, HCT and normal hematological indexes, 21.5 % with only MCV or HCV decreased, 22.5 % patients with HB in value 10.8 g/dl for women and 11.08 g/dl form men, 15 % patients with HB 9.8-10.6g/d L and 9% patients with HB 7.8-9.6, g/d L (mean SD=2,2 ); average number of Reticulocytes =1.2%; Corrected Index Ret = 0.6%; Production Index Reticulocytes, (PIR) = 1.4, meaning the hypo-regenerative anemia with globular value, GV =1.2. Precision: CV < 2% for RBC, CV < 1% for HB and CV < 2% for HCT. Accuracy: R > 0.95 for RBC, HGB and HCT. In this study was observed a higher prevalence of anemia in elderly men than in women. Anemia of renal disease is considered to be a distinct form of anemia and is typical due to decreased EPO production in 20 percent from normal value to adult persons. Discussion: Elderly anemic patients fail to show increases in erythrocytes progenitors and reticuloculocytes as a result of chronic stress along life. In some cases, the presence of anemia may reflect an underling or undetected medical condition.Conclusions: Most anemic adults are asymptomatic until HGB fall below normal values. For this reason a routine anemia screening should be recommended by HB, HCT and MCV, HCV, MCHC to persons with age past >_65 year.

Aging as a consequence of misrepair—A novel theory of aging

Thomas Michelitsch — Mon, 06 Apr 2009 09:27:20 UTC

Aging as a consequence of misrepair—A novel theory of aging

Thomas Michelitsch — Mon, 30 Mar 2009 08:51:45 UTC

It is now increasingly realized that the underlying mechanisms which govern aging is a complex interplay of genetic regulation and damage accumulation. Aging as a result of accumulation of ‘faults’ on cellular and molecular levels, has been proposed in the damage (fault)-accumulation theory by Kirkwood 2006. However, this theory fails to explain some aging phenotypes such as fibrosis and premature aging, since terms such as ‘damage’ and ‘fault’ are not specified. Therefore we introduce here a specification of the underlying mechanism and arrive at a novel theory: aging of the body is a result of the accumulation of Misrepair of tissue. It emphasizes: a) it is Misrepair, not the original damage, that accumulates and leads to aging; and b) aging can occur at different levels, however aging of the body takes place at least on the tissue level, but not necessarily on cellular/molecular level. The novel concept of Misrepair which is introduced here unifies the understanding of the roles of environmental damage, repair, gene regulation, and multicellular structure in the aging process. The Misrepair-accumulation theory which is introduced here gives also explanations for the aging phenotypes, premature aging, and the difference of longevity in different species and is consistent with the point of view of physical theory of complex systems.

Prevalence of sarcopenia and sarcopenic obesity in Korean adults: The Korean Sarcopenic Obesity Study (KSOS)

Tae Nyun Kim — Wed, 04 Mar 2009 21:23:32 UTC

Context: Sarcopenic obesity (SO), a combination of excess weight and reduced muscle mass and/or strength, is suggested to be associated with an increased risk of adverse health outcomes. Objectives: To examine the prevalence and characteristics of Sarcopenic and SO defined by using different indices such as Appendicular Skeletal muscle Mass (ASM)/height2 and Skeletal Muscle Index (SMI (%): skeletal muscle mass (kg)/weight (kg) × 100) for Korean adults. Methods: 591 participants were recruited from the Korean Sarcopenic Obesity Study (KSOS) which is an ongoing prospective observational cohort study. Analysis was conducted in 526 participants (328 women, 198 men) who had complete data on body composition using Dual X-ray absorptiometry and computed tomography. Results: The prevalence of sarcopenia and SO increases with aging. Using two or more standard deviations (SD) of ASM/height2 below reference values from young, healthy adults as a definition of sarcopenia, the prevalence of sarcopenia and SO was 6.3% and 1.3% in men and 4.1% and 1.7% in women over 60 years of age. However, using two or more SD of SMI, the prevalence of sarcopenia and SO was 5.1% and 5.1% respectively in men and 14.2% and 12.5% respectively in women. As defined by SMI, subjects with SO had 3 times the risk of metabolic syndrome (OR = 3.03, 95% confidence interval (CI) = 1.26-7.26) and subjects with non-sarcopenic obesity had approximately 2 times the risk of metabolic syndrome (OR = 1.89, 95% CI = 1.18-3.02) compared with normal subjects. Conclusion: Obese subjects with relative sarcopenia were associated with a greater likelihood for metabolic syndrome. As Koreans were more obese and aging, the prevalence of SO and its impact on health outcomes are estimated to be rapidly grow. Further research is requested to establish the definition, cause and consequences of SO.

Aging-associated Alteration in the Cardiac MIF-AMPK Cascade in Response to Ischemic Stress

Ji Li — Thu, 06 Nov 2008 15:07:20 UTC

An important role for a macrophage migration inhibitory factor (MIF)-AMP-activated protein kinase (AMPK) signaling pathway in ameliorating myocardial damage following ischemia/reperfusion has been described. An aging-associated reduction in AMPK activity may be associated with a decline in the ability of cardiac cells to activate the MIF-AMPK cascade, thereby resulting in reduced tolerance to ischemic insults. To test this hypothesis, in vivo regional ischemia was induced by occlusion of the left anterior descending (LAD) coronary artery in young (4-6 months) and aged (24-26 months) mice. The ischemic AMPK activation response was impaired in aged hearts compared to young ones (p

D-aspartate exerts an opposing role upon age-dependent NMDAR-related synaptic plasticity and memory decay

Alessandro Usiello — Thu, 15 May 2008 13:41:48 UTC

In the present study, we demonstrated that D-aspartate acts as an in vitro and in vivo neuromodulatory molecule upon hippocampal NMDAR transmission. Accordingly, we showed that this D-amino acid, widely expressed during embryonic phase, was able to strongly influence hippocampus-related functions at adulthood. Thus, while up-regulated levels of D-aspartate increased LTP and spatial memory in four-month old adult mice, the prolonged deregulation of this molecule in thirteen-month old animals induced a substantial acceleration of age-dependent decay of synaptic plasticity and cognitive functions. Moreover, we highlighted a role for D-aspartate in enhancing NMDAR-dependent synaptic plasticity through an inducible "turn-on/turn-off-like mechanism". Strikingly, we also showed that D-aspartate, when administered to aged mice, strongly rescued their physiological synaptic decay and attenuated their cognitive deterioration. In conclusion, our data suggest a tantalizing hypothesis for which this in-embryo-occurring D-amino acid, might disclose plasticity windows in the aging brain.