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Background: Cognitive decline and dementia represent a key problem for public health as they heavily impair social functioning and independent living. The development of new strategies to support recommendations for patients and their caregivers may represent an outstanding step forward. Aims: To describe the study protocol and methods of 'My Mind Project: the effect of cognitive training for elderly' (Grant No. 154/GR-2009-1584108), which investigates, by the use of a multidisciplinary approach, the effects of a comprehensive cognitive training programme on performances in aged subjects with mild-moderate Alzheimer's disease, mild cognitive impairment and normal cognitive functioning. Methods: The study is a prospective randomized intervention for the assessment of cognitive training effects in three groups of elderly subjects with different cognitive status. A total of 321 elderly people were enrolled in Marche Region, Italy. Each subject was randomly assigned to an experimental group or to a control group. Cognitive performances and biochemical blood markers have also been analysed before cognitive training (baseline), immediately after termination (follow-up 1), after 6 months (follow-up 2) and after 2 years (follow-up 3). Discussion: The results will be useful to identify some efficient programmes for the enhancement of cognitive performance in elderly with and without cognitive decline. Conclusion: The application of a non-pharmacological approach in the treatment of elderly with cognitive disorders could have a profound impact on National Health Service. [ABSTRACT FROM AUTHOR]

Objectives: To assess the effect of mild forced physical training on cerebral blood volume (CBV) and other brain parameters in old mice. Setting: Treadmill in the animal house. Participants: Thirty old (>25 mo) male mice were randomly assigned to one of three groups, exercise (E), exercise plus testosterone (T) (ET), and rest (C). Intervention: Mild physical training on treadmill (30 min a day at belt speed = 8 m/min, five days a week) with or without one weekly injection of testosterone. Measurements: CBV, quantitative transverse relaxation time (T2) maps, and cortical thickness were measured by magnetic resonance imaging. Results: A significant increase of CBV was found in the motor and hippocampal cortex of E and ET mice; cortical thickness was not affected. T2 maps analysis suggested that water distribution did not change. T administration did not add to the effect of physical training. Conclusion: This work provides first quantitative evidence that exercise initiated at old age is able to improve the hemodynamic status of the brain cortex in key regions for movement and cognition without inducing edema. [ABSTRACT FROM AUTHOR]

The precise cause of sarcopenia, skeletal muscle loss and strength, in older persons is unknown. However, there is a strong evidence for muscle loss due to insulin resistance as well as mitochondrial dysfunction over aging. Considering that epidemiological studies have underlined that insulin resistance may have a specific role on skeletal muscle fibre atrophy and mitochondrial dysfunction has also been extensively shown to have a pivotal role on muscle loss in older persons, a combined pathway may not be ruled out. Considering that there is growing evidence for an insulin-related pathway on mitochondrial signaling, we hypothesize that a high degree of insulin resistance will be associated with the development of sarcopenia through specific alterations on mitochondrial functioning. This paper will highlight recent reviews regarding the link between skeletal muscle mitochondrial dysfunction and insulin resistance. We will specifically emphasize possible steps involved in sarcopenia over aging, including potential biomolecular mechanisms of insulin resistance on mitochondrial functioning. [ABSTRACT FROM AUTHOR]

We measured the effect of chronic ethanol administration on the expression of Glut3 in the cerebellum and hippocampus of adult and old rats. Glut3 expression significantly decreased in aging, in ethanol-treated rats vs. age-matched controls, and in adult- vs. old ethanol-treated rats. These findings lend consistent support to the hypothesis that disturbances of glucose metabolism due to ethanol may constitute an unfavorable condition predisposing to neuronal death. [ABSTRACT FROM AUTHOR]

Background: Nerve endings undergo a lifespan morphofunctional modulation which is reported to be markedly impaired with aging. Neurone structural remodelling is in charge of processes occurring in the nerve cell soma, however the axonal transportation of organelles and molecules by cytoskeletal elements plays a very important role in the morphological rearrangements taking place at peripheral compartments.Objective: To assess the involvement of axonal ultrastructure in the reported age-related decline of slow axoplasm flow mechanisms, we carried out a morphometric study of axon cytoskeleton in aging.Methods: Female Wistar rats (3, 12 and 30 months of age) were anesthetized and perfused with saline followed by a fixation solution (glutaraldehyde 5% + formalin 2% in 0.1 cacodylate buffer pH 7.4). The excised sciatic nerves were processed according to conventional electron microsopic procedures. Axons sectioned perpendicularly to their longitudinal axis at the internodal region (mean axoplasm area: 18.25-26.5 microm(2)) were sampled by a systematic random procedure. The overall number of neurofilaments (No.Nfs) and microtubules (No.Mts) per total axoplasm area analysed, the numeric density (number/microm(2) of axoplasm area) of neurofilaments (NaNfs) and microtubules (NaMts), the myelin thickness, the number of myelin lamellae and the R proportion [No. Nfs/(No.Nfs + No.Mts)] were the parameters measured by computer-assisted semiautomatic methods.Results: No.Nfs, NaNfs, myelin thickness and the number of myelin lamellae did not change between 12 and 30 months of age, while a significant increase of these parameters was found in a comparison with younger rats. No.Mts and NaMts were significantly increased at 12 vs. 3 as well as at 30 vs. 12 months of age, respectively. R proportion did not show any difference due to age.Conclusions: The present findings support that the dynamic condition of the axonal cytoskeleton appears to be preserved at a high extent in aging. Thus, the intra-axonal defective spacing of cytoskeletal elements (e.g. neurofilaments), rather than their number, is proposed to contribute to the decline of the slow axonal transport of organelles and molecules reported in aging. [ABSTRACT FROM AUTHOR]