Omega-3 Fatty Acids in Early Prevention of Inflammatory Neurodegenerative Disease: A Focus on Alzheimer's Disease.

Alzheimer's disease (AD) is the leading cause of dementia and the most common neurodegenerative disease in the elderly. Furthermore, AD has provided the most positive indication to support the fact that inflammation contributes to neurodegenerative disease. The exact etiology of AD is unknown, but environmental and genetic factors are thought to contribute, such as advancing age, family history, presence of chronic diseases such as cardiovascular disease (CVD) and diabetes, and poor diet and lifestyle. It is hypothesised that early prevention or management of inflammation could delay the onset or reduce the symptoms of AD. Normal physiological changes to the brain with ageing include depletion of long chain omega-3 fatty acids and brains of AD patients have lower docosahexaenoic acid (DHA) levels. DHA supplementation can reduce markers of inflammation. This review specifically focusses on the evidence in humans from epidemiological, dietary intervention, and supplementation studies, which supports the role of long chain omega-3 fatty acids in the prevention or delay of cognitive decline in AD in its early stages. Longer term trials with long chain omega-3 supplementation in early stage AD are warranted. We also highlight the importance of overall quality and composition of the diet to protect against AD and dementia.

Mode of molecular recognition of L-fucose by fucose-binding legume lectins.

Recognition of cell surface carbohydrate moieties by lectins plays a vital role in many a biological process. Fucosyated residues are often implicated as key recognition markers in many cellular processes. In particular, the aspects of molecular recognition of fucose by fucose-bindinglectins UEA 1 and LTA pose a special case because no crystal structure of these lectins is available. The study was conducted to elucidate the process of recognition of l-fucose by UEA1 and LTA by correlating structure-based sequence alignment and other available biochemical/biophysical data. The study points out that the mode of recognition of l-fucose is coordinated by the invariant triad of residues the asparagine 137, glycine 105, and aspartate 87. The major hydrophobic stacking residue in this case is the tyrosine 220. The study also reiterates the key role of the conserved triad of residues in the combining site which is a common feature for all legume lectins whose crystal structures are known.

Microbial spoilage of pre-cooked potato-topped pies.

The ecological succession of bacteria which developed in pre-cooked potato-topped pies stored at two different temperatures was examined. Bacillus, Streptococcus and Staphylococcus-Micrococcus spp. were the predominant organisms isolated from freshly prepared pies and those stored at 4 degrees and 37 degrees C. None of these groups of bacteria caused significant biodeterioration of pies held at 4 degrees C, but all groups grew well in pies stored at 37 degrees C and achieved counts of ca 10(8)/g of sample. Bacillus spp. were the first group to grow, followed by Streptococcus and Staphylococcus-Micrococcus spp. Growth which occurred at 37 degrees C did so at the expense of glucose, lactate accumulated and the pH of pie components decreased. Amylase activity detected in all pie components during storage was associated with the growth of Bacillus spp. and probably supplemented glucose already present in pies, by hydrolytic cleavage of potato, flour or binder starches. Spoilage caused by growth and activity of the bacteria isolated was not associated with visual signs of biodeterioration, nor production of 'off' odour usually associated with spoilage of meats. These results suggest that pre-cooked potato-topped pies held at inappropriate temperatures represent a potential public health risk.

Vitamin D metabolites and parathyroid hormone in Cushing's syndrome: relationship to calcium and phosphorus homeostasis.

We studied the effects of glucocorticoid excess on calcium and phosphorus homeostasis in relation to vitamin D metabolites and parathyroid hormone (PTH) in seven patients with spontaneous ACTH-dependent Cushing's syndrome. Remission of hypercortisolism resulted in a significant increase in tubular reabsorption of phosphate [from 76 +/- 4% to 89 +/- 2% (mean +/- SEM); P less than 0.01] and serum phosphorus (from 3.1 +/- 0.1 to 4.2 +/- 0.2 mg/dl; P less than 0.005). Serum calcium did not change, although there was a reduction in daily urinary calcium excretion from 0.23 +/- 0.02 to 0.107 +/- 0.02 mg calcium/mg creatinine. Serum immunoreactive PTH (iPTH) levels were normal during Cushing's syndrome (34 +/- 5 microleq/ml), but fell significantly after remission to 22 +/- 2 microleq/ml (P less than 0.05). This small decrease in iPTH did not correlate with the improvement of phosphate homeostasis. Plasma 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D [1,25-(OH2)D] concentrations in Cushing's syndrome did not differ from measurements in 97 normal subjects. After treatment, 25OHD did not change, but 1,25-(OH)2D fell in each patient from a mean of 44 to 22 pg/ml (P less than 0.02). 1,25-(OH)2D was inversely correlated with serum phosphorus (r = 0.59; P less than 0.01), but did not correlate with iPTH. The known impairment of intestinal calcium absorption in Cushing's syndrome cannot be attributed to a decrease in the circulating levels of 1,25-(OH)2D. Endogenous hypercortisolism decreases tubular phosphate reabsorption and serum phosphorus, increase tubular phosphate reabsorption and serum phosphorus, increases iPTH, and results in an increase in 1,25-(OH)2D. These events may contribute to the severe loss of bone mass in such patients and may account for the calciuria and phosphaturia of Cushing's syndrome.