Organ Size

Publication Title: 
Folia Morphologica

A comparison of the data published in anatomy textbooks and anthropological tables does not reveal any change in basic heart dimensions during the period since the beginning of the 20th century to nowadays. However, normal values of many other parameters have changed up to 30% over the same period. These changes may be caused by the acceleration phenomenon or the extension of average lifespan.

Author(s): 
Skwarek, M.
Grzybiak, M.
Kosi?ski, A.
Hreczecha, J.
Publication Title: 
Journal of the Neurological Sciences

Amyotrophic lateral sclerosis (ALS) is a progressive disease which is caused by degeneration of motor neurons in the central nervous system. The incidence of ALS is higher in men than women, but the female advantage disappears with increased age. Here, we report evidence that the female advantage is due to the protective role of estrogen. In an ALS mouse model carrying the human Cu/Zn superoxide dismutase (hSOD1) G93A transgene, ovariectomy did not alter the onset age of the disease while reducing the female lifespan by 7 days and making it comparable to that of the male transgenic mice.

Author(s): 
Choi, Chan-Il
Lee, Young-Don
Gwag, Byoung Joo
Cho, Sung Ig
Kim, Sung-Soo
Suh-Kim, Haeyoung
Publication Title: 
Human Molecular Genetics

Spinal muscular atrophy (SMA) is the most common genetic cause of infant mortality. SMA is caused by loss of functional survival motor neuron 1 (SMN1), resulting in death of spinal motor neurons. Current therapeutic research focuses on modulating the expression of a partially functioning copy gene, SMN2, which is retained in SMA patients. However, a treatment strategy that improves the SMA phenotype by slowing or reversing the skeletal muscle atrophy may also be beneficial. Myostatin, a member of the TGF-beta super-family, is a potent negative regulator of skeletal muscle mass.

Author(s): 
Rose, Ferrill F.
Mattis, Virginia B.
Rindt, Hansjˆrg
Lorson, Christian L.
Publication Title: 
Aging Cell

Atrophy is one of the major age-related changes in the brain. The absence of brain atrophy in elderly individuals reflects deceleration in the process of biological aging. Moreover, results from human twin studies suggest a large genetic influence on the variance of human brain tissue volumes. To investigate the association of brain volumes with exceptional longevity, we tested whether middle-aged to elderly offspring of nonagenarian siblings have larger brain volumes than their spouses using magnetic resonance imaging.

Author(s): 
Altmann-Schneider, Irmhild
de Craen, Anton J. M.
Slagboom, Pieternella E.
Westendorp, Rudi G. J.
van Buchem, Mark A.
Maier, Andrea B.
van der Grond, Jeroen
Publication Title: 
Ageing Research Reviews

Life's timekeeper is a 'free-running' intracellular oscillator synchronised across all cells. It runs throughout life splitting lifespan into equal length phases. During the maturational period it controls the overall rate of progression whereas in the post-maturational period it controls the overall rate of ageing. This includes the rate of senescence and hence time to death. As such life's timekeeper equates maturational and post-maturational time, hence explains the tight correlation between these time periods that has existed throughout mammalian evolution.

Author(s): 
Neill, David
Publication Title: 
PloS One

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the selective loss of motor neurons in the spinal cord, brain stem, and motor cortex. Mutations in superoxide dismutase (SOD1) are associated with familial ALS and lead to SOD1 protein misfolding and aggregation. Here we show that the molecular chaperone, HSJ1 (DNAJB2), mutations in which cause distal hereditary motor neuropathy, can reduce mutant SOD1 aggregation and improve motor neuron survival in mutant SOD1 models of ALS.

Author(s): 
Novoselov, Sergey S.
Mustill, Wendy J.
Gray, Anna L.
Dick, James R.
Kanuga, Naheed
Kalmar, Bernadett
Greensmith, Linda
Cheetham, Michael E.
Publication Title: 
Clinics in Endocrinology and Metabolism
Author(s): 
Merry, B. J.
Phillips, J. G.
Publication Title: 
Annual Review of Nutrition
Author(s): 
Emken, E. A.
Publication Title: 
Free Radical Biology & Medicine

Energy restriction (ER), without malnutrition, increases maximum life span and retards the development of a broad array of pathophysiological changes in laboratory rodents. The mechanism responsible for the retardation of aging by ER is, however, unknown. One proposed explanation is a reduction in energy expenditure (EE). Reduced EE may increase life span by decreasing the number of oxygen molecules interacting with mitochondria, thereby lowering reactive oxygen species (ROS) production. As a step toward testing this hypothesis, it is important to determine the effect of ER on EE.

Author(s): 
Ramsey, J. J.
Harper, M. E.
Weindruch, R.
Publication Title: 
Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et MÈtabolisme

We examined the effects of diets based on a low isoflavone or a high isoflavone soy protein isolates in normal, growth-hormone receptor knockout and Ames dwarf, and Prop 1 (df) mice that are hypoinsulinemic, insulin-sensitive, and exceptionally long-lived, as well as in growth hormone transgenic mice that are hyperinsulinemic, insulin-resistant, dyslipidemic, and short-lived. Soybean diets tended to normalize plasma cholesterol levels in dwarf and transgenic mice, while low isoflavone diet reduced plasma triglycerides in most of the examined genotypes.

Author(s): 
Bartke, A.
Peluso, M. R.
Moretz, N.
Wright, C.
Bonkowski, M.
Winters, T. A.
Shanahan, M. F.
Kopchick, J. J.
Banz, W. J.

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