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Exposure to high levels of aluminium (Al) leads to neurofibrillary degeneration and that Al concentration is increased in degenerating neurons in Alzheimer's disease (AD). Nevertheless, the role of Al in AD remains controversial and there is little proof directly interlinking Al to AD. The major problem in understanding Al toxicity is the complex Al speciation chemistry in biological systems. A new dimension is provided to show that Al-maltolate treated aged rabbits can be used as a suitable animal model for understanding the pathology in AD. The intracisternal injection of Al-maltolate into aged New Zealand white rabbits results in pathology that mimics several of the neuropathological, biochemical and behavioural changes as observed in AD. The neurodegenerative effects include the formation of intraneuronal neurofilamentous aggregates that are tau positive, oxidative stress and apoptosis. The present review discusses the role of Al and use of Al-treated aged rabbit as a suitable animal model to understand AD pathogenesis.

Background & Objective: Drugs like famotidine, omeprazole and sucralfate which have been reported to promote the healing of gastric ulcers, may have the same effect on cutaneous wounds. Due to paucity of information in this regard, the present study was planned to investigate the effect of these drugs on resutured incision, excision and dead space wounds in Wistar rats., Methods: Resutured incision, excision and dead space wounds were inflicted under light ether anaesthesia aseptically. Control animals received vehicle and other groups received famotidine, omeprazole and sucralfate orally for a period of 10 days in the incision and dead space wounds, whereas in excision wounds till complete closure. On the 11th day after estimating breaking strength of the resutured incision wounds, animals were sacrificed and granulation tissue removed from dead space wounds to estimate the breaking strength and hydroxyproline content. Quantification of granulation tissue and histological studies were also carried out. Wound closure rate, epithelization time and scar features were studied in the excision wound models from the day of famotidine till complete closure of the wound., Results: Only famotidine significantly promoted the healing process in all the three wound models studied. Histopathological studies revealed increased collagen content and granulation tissue in famotidine treated group compared to control., Interpretation & Conclusion: In all the three wound models studied famotidine promoted wound healing whereas omeprazole and sucralfate did not do so. The pro healing effect of famotidine needs to be explored clinically.

The validity of DNA damage and repair hypothesis of ageing has been examined with special reference to the brain. As far as the accumulation of DNA damage is concerned, the data appear to overwhelmingly support the hypothesis. However, the results of attempts to demonstrate a decline in DNA repair capacity as a function of age are conflicting. However, more recent observations are in support of age-dependent deterioration in DNA-repair capacity. Possible reasons for this discrepancy and the usefulness of conducting DNA damage and repair studies in a model system of isolated neuronal cells, are discussed. It is suggested that assessment of repair capacity of brain with respect to a specific damage in a designated gene might yield more definitive answers regarding the role of DNA repair potential in the ageing process and as a longevity assurance system.

Effect of protein deficiency, which was produced in rats either by feeding low protein diet (8% protein) ad libitum (PD) or by restricting the amount of diet containing 15 per cent protein (protein calorie deficiency; PCD) on the growth in terms of muscle weight, length, cross-sectional area, protein and glycogen content was studied in extensor digitorum longus (EDL), medial gastrocnemius (MG) and plantaris (PL) muscles in rat. Because of decreased total calorie intake, PCD group exhibited higher value for protein/total calorie consumption. Excepting glycogen concentration, the retardation of growth in terms of all parameters studied was less in the PCD group. Glycogen concentration (mg/g muscle weight) in the PCD group was 3.0 +/- 0.3 in EDL and 2.6 +/- 0.3 in PL, whereas the values in PD group were 1.0 +/- 0.1 in EDL and 1.1 +/- 0.2 in PL respectively. This glycogen sparing effect was not evident in MG of PCD group possibly due to the greater number of glycolytic fibres. It is suggested that lesser retardation of growth of muscles and glycogen sparing effect in PCD group, could be due to altered metabolic changes resulting in enhanced gluconeogenesis.