Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0751295 (memory loss)
 3,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Type 2 diabetes mellitus (DM) is associated with increased incidence of behavioral changes and memory loss. Memory loss could be caused by Alzheimer's disease (AD) and vascular dementia (VaD). So, we aimed to investigate the effect of sitagliptin in improving the working and reference memories in diabetic rats. Thirty six male Sprague-Dawley rats divided equally (n=12) into three groups: control, type 2 DM and type 2 DM treated with DPP-4 inhibitor (sitagliptin) for one month (10 mg/kg) orally. Working memory and reference memory were assessed by using the holeboard memory test. In all rats, serum glucose, insulin, adiponectin, total cholesterol (TC), TG, low (LDL) and high (HDL) density lipoprotein with calculation of the homeostasis model of assessment-insulin resistance index (HOMA-IR) and atherogenic index. The hypothalamus was separated for determination of the acetylcholine level and adiponectin receptors 1 (Adipo R1) m-RNA expression. Type 2 diabetic rats exhibited a significant decrease in both working and reference memories, with increased glucose, insulin and HOMA-IR. The adiponectin level, acetylcholine content of the hypothalamus and Adipo R1 m-RNA expression were significantly reduced. Treatment with sitagliptin significantly improved the working and reference memories with significant reduction in the glucose, insulin and HOMA-IR. Moreover, sitagliptin increased significantly the acetylcholine content of the hypothalamus and Adipo R1 expression. In conclusion, sitagliptin might improve the cognitive function of the diabetic rats and the hypothalamic acetylcholine level possibly through increased AdipoR1 expression.
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PMID:Effect of sitagliptin on the working memory and reference memory in type 2 diabetic Sprague-Dawley rats: possible role of adiponectin receptors 1. 2430 75

Alzheimer's disease is a major neurodegenerative disease characterized by memory loss and cognitive deficits. Recently, we reported that osmotin, which is a homolog of adiponectin, improved long-term potentiation and cognitive functions in Alzheimer's disease mice. Several lines of evidence have suggested that Nogo-A and the Nogo-66 receptor 1 (NgR1), which form a complex that inhibits long-term potentiation and cognitive function, might be associated with the adiponectin receptor 1 (AdipoR1), which is a receptor for osmotin. Here, we explore whether osmotin's effects on long-term potentiation and memory function are associated with NgR1 signaling via AdipoR1 in Alzheimer's disease. Osmotin reduced the expression of NgR1 without affecting Nogo-A expression. Furthermore, osmotin inhibited NgR1 signaling by prohibiting the formation of the Nogo-A and NgR1 ligand-receptor complex, resulting in enhanced neurite outgrowth; these effects disappeared in the presence of AdipoR1 interference. In addition, osmotin increased the expression of the pre- and postsynaptic markers synaptophysin and PSD-95, as well as the activation of the memory-associated markers AMPA receptor and CREB; these effects occurred in an AdipoR1- and NgR1-dependent manner. Osmotin was also found to enhance dendritic complexity and spine density in the hippocampal region of Alzheimer's disease mouse brains. These results suggest that osmotin can enhance neurite outgrowth and synaptic complexity through AdipoR1 and NgR1 signaling, implying that osmotin might be an effective therapeutic agent for Alzheimer's disease and that AdipoR1 might be a crucial therapeutic target for neurodegenerative diseases such as Alzheimer's.
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PMID:The Adiponectin Homolog Osmotin Enhances Neurite Outgrowth and Synaptic Complexity via AdipoR1/NgR1 Signaling in Alzheimer's Disease. 2933 44

Introduction Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative disease. Typical features of AD include memory loss, social dysfunction and physical impairment. Although the pathological findings in the central nervous system are well established, the etiological factors are poorly known. Recent studies suggested the role of metabolic disturbances in the development of AD neurodegeneration. Adiponectin, an anti-inflammatory and metabolism regulating factor, was linked to AD. Aim The aim was to examine whether adiponectin fractions combined with insulin/insulin resistance-associated metabolic parameters correlate with AD progression. Material and methods The study comprised 98 women: 27 with moderate to severe AD, 31 with AD at early stage and 40 healthy controls, matched for age and BMI. To evaluate memory impairment, the MMSE was performed. Plasma total adiponectin and its high-, medium- and low molecular weights were measured with ELISA. Anthropometric, clinical and metabolic parameters were assessed. Correlations between adiponectin array and measured parameters were evaluated. Results In comparison to the controls, enhanced levels of total and medium molecular weight adiponectin characterized AD individuals. In AD, we found correlations between adiponectin array, and anthropometric and biochemical parameters. After adjustment to BMI, a significant increase of the total adiponectin and high- and medium molecular weight fractions was observed. A negative correlation between low molecular weight adiponectin and MMSE was found. Conclusions Our results indicate a possible link between adiponectin variations and AD. We hypothesize that changes in adiponectin profile observed in AD result from compensatory mechanism against neuropathological processes, as well as from adiponectin homeostasis impairment.
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PMID:Plasma adiponectin array in women with Alzheimer's disease. 3011 32