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Cognitive impairments and cholinergic dysfunctions have been well reported in old age disorders including Alzheimer’s disease (AD). d -galactose (D-gal) has been reported as a senescence agent while aluminium act as a neurotoxic metal, but little is known about their combined effects at different doses. The aim of this study was to establish an animal model with cognitive impairments by comparing the effects of different doses of co-administrated D-gal and aluminium chloride (AlCl 3 ). In this study male albino wistar rats were administered with D-gal 60 mg/kg.bwt intra peritoneally (I.P) injected and AlCl 3 (100, 200, or 300 mg/kg.bwt.) was orally administered once daily for 10 consecutive weeks. Performance of the rats were evaluated through behavioural assessments; Morris water maze (MWM) and open field tests (OFT); histopathological examination was performed on the hippocampus; moreover biochemical measurements of acetylcholinesterase (AChE) and hyperphosphorylated tau protein (p-tau) were examined. The results of this experiment on rats treated with D-gal 60 + AlCl 3 200 mg/kg.bwt showed near ideal cognitive impairments. The rats exhibited an obvious memory and learning deficits, marked neuronal loss in hippocampus, showed increase in AChE activities and high expression of p-tau within the tissues of the brain. This study concludes that D-gal 60 + AlCl 3 200 mg/kg.bwt as the ideal dose for mimicking AD like cognitive impairments in albino wistar rats. It is also crucial to understand the pathogenesis of this neurodegenerative disease and for drug discovery. [ABSTRACT FROM AUTHOR]

Context:Morus nigraL. (Moraceae) has various uses in traditional medicine. However, the effect ofM. nigraon cognitive impairment has not been investigated yet. Objective: The objective of this study is to determine the phenolic acid content and DNA damage protection potential ofM. nigraleaf extract and to investigate the extract effect on cognitive impairment and oxidative stress in aging mice. Materials and methods: Phenolic acid content was determined by quantitative chromatographic analysis. DNA damage protection potential was evaluated on pBR322 plasmid DNA. Thirty-two Balb-C mice were randomly divided into four groups (control,d-galactose,d-galactose + M. nigra50, andd-galactose + M. nigra100). Mice were administeredd-galactose (100 mg/kg, subcutaneous) andM. nigra(50 or 100 mg/kg, orally) daily for 8 weeks. Behavioral responses were evaluated with Morris water maze. Activities of antioxidant enzymes and levels of malondialdehyde (MDA) were assayed in serum, brain, and liver. Results: In extract, vanillic (632.093 μg/g) and chlorogenic acids (555.0 μg/g) were determined. The extract between 0.02 and 0.05 mg/mL effectively protected all DNA bands against the hazardous effect of UV and H2O2.Morus nigrasignificantly improved learning dysfunctions (p < 0.01), increased memory retention (p < 0.01), reduced MDA levels (p < 0.05), and elevated SOD, GPx, and CAT activities (p < 0.05) compared with thed-galactose group. Discussion and conclusion: These results show thatM. nigrahas the potential in improving cognitive deficits in mice and thatM. nigramay be useful to suppress aging, partially due to its scavenging activity of free radicals and high antioxidant capacity. [ABSTRACT FROM AUTHOR]

Abstract: Basic and clinical research has demonstrated that dementia of sporadic Alzheimer's disease (sAD) type is associated with dysfunction of the insulin-receptor (IR) system followed by decreased glucose transport via glucose transporter GLUT4 and decreased glucose metabolism in brain cells. An alternative source of energy is d-galactose (the C-4-epimer of d-glucose) which is transported into the brain by insulin-independent GLUT3 transporter where it might be metabolized to glucose via the Leloir pathway. Exclusively parenteral daily injections of galactose induce memory deterioration in rodents and are used to generate animal aging model, but the effects of oral galactose treatment on cognitive functions have never been tested. We have investigated the effects of continuous daily oral galactose (200 mg/kg/day) treatment on cognitive deficits in streptozotocin-induced (STZ-icv) rat model of sAD, tested by Morris Water Maze and Passive Avoidance test, respectively. One month of oral galactose treatment initiated immediately after the STZ-icv administration, successfully prevented development of the STZ-icv-induced cognitive deficits. Beneficial effect of oral galactose was independent of the rat age and of the galactose dose ranging from 100 to 300 mg/kg/day. Additionally, oral galactose administration led to the appearance of galactose in the blood. The increase of galactose concentration in the cerebrospinal fluid was several times lower after oral than after parenteral administration of the same galactose dose. Oral galactose exposure might have beneficial effects on learning and memory ability and could be worth investigating for improvement of cognitive deficits associated with glucose hypometabolism in AD. [Copyright &y& Elsevier]

Objectives: To study and compare the effects of fructose and galactose on, blood glucose, insulin, Hb1cand lipids and anthropometric measurements. Data Source: Ninety, 1c healthy adult male rats of Sprague-Dawley strain. Design: Experimental study. Setting: Department of Biochemistry and Molecular Biology, A.M.C, Rawalpindi, in collaboration with N.I.H, Islamabad. Period: Twelve months. Subjects and Methods: Rats weighing 180-350 grams were selected by random sampling and were divided into three groups, 30 each. Group I was given standard diet, Group II was given high fructose diet (HFD), i.e., 1.5gms/Kg body weight/day of fructose, along with standard diet for two weeks and Group III was given high galactose diet, i.e., 0.83gms/Kg body weight/day, along with standard diet for two weeks. Results: There was a significant increase in height of galactose group while fructose group has significant weight loss; BMI decreased in both but more in former. The blood levels of cholesterol, HDL-c, LDL-c, TG, and insulin were significantly higher in fructose group than in galactose group. There was no significant difference between blood glucose and HbA1c among these groups yet their higher levels indicate the chances of developing insulin resistance. Conclusions: Fructose due to its less hyperglycaemic effects should not be used in diet and must not be prescribed in diabetes, as in the long run it can lead to obesity, hypertension and cardiovascular risk. Non-significant effects of galactose on above parameters (except lipoproteins), does not mean that it can be used as an alternative to fructose and this area needs exploration. [ABSTRACT FROM AUTHOR]

Abstract: The biosynthesis of l-ascorbic acid (AsA) in tomato (Solanum lycopersicum cv. Money Maker) hairy roots (HR) was studied, by quantification of total intracellular AsA during 35 days of batch culture and by evaluation of the effects of potential biosynthetic precursors on AsA concentrations. Two types of tomato HR were used in order to asses the possible functional pathways of vitamin C biosynthesis in isolated roots: wild type (WT) and transgenic HR overexpressing GalUR gene. GalUR codifies a d-galacturonic acid reductase (EC 1.1.1.19) from strawberry fruit, involved in the galacturonate pathway for AsA biosynthesis. Our results show that completely isolated tomato roots are able to synthesize AsA in situ and de novo during 35 days, and that AsA accumulates in the roots in a non-growth-associated manner. Feeding the roots with d-galactose (d-Gal) or d-galacturonic acid (d-GalUA) produced a time- and dose-dependent increase in total AsA content in both types of tomato HR clones. An increase of 2.5-fold in total AsA content was observed in a transgenic HR clone treated with d-GalUA compared with the basal AsA content of the WT one. These results show evidences that at least the galacturonate pathway could operate in isolated wild type and transgenic tomato roots, and that bioavailability of such precursors in roots could be limiting AsA biosynthesis. [Copyright &y& Elsevier]

Multiple cases of IgA nephropathy (IgAN) may occur in families; we compared their prognosis to sporadic cases of this disease. We isolated macromolecular IgA1 from 60 patients with familial IgAN, 91 of their asymptomatic relatives, 43 patients with sporadic IgAN (SpIgAN), 90 of their asymptomatic relatives, and 43 healthy subjects. Compared with SpIgAN patients, those with multiplex familial IgAN (MpIgAN) had more advanced renal histopathology and more galactose-deficient macromolecular IgA1 in their serum. Further, when we tested the effects of the macromolecular IgA1 on human mesangial cells in culture, we found that the macromolecular IgA1 taken from familial clusters had enhanced binding to mesangial cells and caused increased expression of interleukin-6, tumor necrosis factor-α, and monocyte chemotactic peptide-1. The macromolecular IgA1 isolated from asymptomatic relatives caused increased cytokine expression in the mesangial cells when derived from MpIgAN compared with SpIgAN or healthy controls. While these studies suggest that macromolecular IgA1 isolated from patients with MpIgAN is more pathogenic than that from patients with SpIgAN, long term follow-up will be needed to clarify the risk in asymptomatic relatives of the patients with multiplex familial disease.Kidney International (2009) 75, 1330–1339; doi:10.1038/ki.2009.71; published online 1 April 2009 [ABSTRACT FROM AUTHOR]

Reviews the article `Lactose and galactose intake and metabolism in relation to the risk of epithelial ovarian cancer,' by L.J. Herrinton et al published in the March 1, 1995 issue of the `American Journal of Epidemiology.'