際際滷shows by User: TosifaMemon / http://www.slideshare.net/images/logo.gif 際際滷shows by User: TosifaMemon / Mon, 21 Jan 2013 18:48:21 GMT 際際滷Share feed for 際際滷shows by User: TosifaMemon Proposed mechanism underlying the therapeutic effects of withania somnifera in alzheimers disease /slideshow/proposed-mechanism-underlying-the-therapeutic-effects-of-withania-somnifera-in-alzheimers-disease/16106254 proposedmechanismunderlyingthetherapeuticeffectsofwithaniasomniferainalzheimersdisease-130121184821-phpapp02
I am Tosifa Memon, currently a phD candidate in Biology department at the University of Utah. I worked on this proposal for my qualifying exam and got the opportunity to present it to my thesis committee. Abstract: The root extract of Withania somnifera (WS), traditionally known to enhance memory, has been reported to improve cognitive and behavioral deficits in mice models of Alzheimers disease (AD). WS treatment was also found effective in reducing brain depositions and promoting peripheral clearance of toxic amyloid- (A) peptides which can otherwise interfere with normal neuronal function. How WS treatment exerts these beneficial effects remains unexplored and demands further investigation. Interestingly, Sehgal et al. study also found that WS treatment enhanced expression of liver low density lipoprotein-related protein (LRP1) along with plasma soluble form of LRP (sLRP), key players in peripheral A硫 clearance. Conversely, downregulation of liver LRP1 abrogated the therapeutic effects of WS extract and reduced plasma sLRP level. This finding not only highlights LRP1 as a potential target in AD treatment but also hints at WS components as potential leads for drug discovery. Therefore, it is imperative to know how treatment with WS root extract induces liver LRP1 expression. WS extract possesses hypocholesteremic and hypoglycemic activity. This may offer some explanation to therapeutic effects of WS treatment as abnormal cholesterol metabolism and insulin-resistance are known risk-factors in AD onset and progression. Like WS extract, cholesterol and insulin can also regulate LRP1 expression. Depletion in cell cholesterol, most likely by inhibiting bile acid (BA) reabsorption, can upregulate LRP1 mRNA expression and sLRP release while insulin stimulation promotes translocation of LRP1 from cytosol to plasma membrane (PM). Therefore, it is possible that WS induces LRP1 mRNA expression and sLRP release by inhibiting intestinal BA reabsorption and consequent depletion in liver cell cholesterol. In addition, effective peripheral Aclearance by WS will depend on PM expression of liver LRP1 more than its mRNA expression. Hence, it is possible that WS treatment promotes LRP1 translocation to PM by improving insulin signaling and sensitivity. Aim 1: To determine whether treatment with WS inhibits intestinal BA reabsorption leading to reduced cell cholesterol and increased LRP1 expression in liver cells Aim 2: To determine whether treatment with WS improves insulin sensitivity and signalling leading to enhanced liver LRP1 PM expression and A uptake from plasma. ]]>
I am Tosifa Memon, currently a phD candidate in Biology department at the University of Utah. I worked on this proposal for my qualifying exam and got the opportunity to present it to my thesis committee. Abstract: The root extract of Withania somnifera (WS), traditionally known to enhance memory, has been reported to improve cognitive and behavioral deficits in mice models of Alzheimers disease (AD). WS treatment was also found effective in reducing brain depositions and promoting peripheral clearance of toxic amyloid- (A) peptides which can otherwise interfere with normal neuronal function. How WS treatment exerts these beneficial effects remains unexplored and demands further investigation. Interestingly, Sehgal et al. study also found that WS treatment enhanced expression of liver low density lipoprotein-related protein (LRP1) along with plasma soluble form of LRP (sLRP), key players in peripheral A硫 clearance. Conversely, downregulation of liver LRP1 abrogated the therapeutic effects of WS extract and reduced plasma sLRP level. This finding not only highlights LRP1 as a potential target in AD treatment but also hints at WS components as potential leads for drug discovery. Therefore, it is imperative to know how treatment with WS root extract induces liver LRP1 expression. WS extract possesses hypocholesteremic and hypoglycemic activity. This may offer some explanation to therapeutic effects of WS treatment as abnormal cholesterol metabolism and insulin-resistance are known risk-factors in AD onset and progression. Like WS extract, cholesterol and insulin can also regulate LRP1 expression. Depletion in cell cholesterol, most likely by inhibiting bile acid (BA) reabsorption, can upregulate LRP1 mRNA expression and sLRP release while insulin stimulation promotes translocation of LRP1 from cytosol to plasma membrane (PM). Therefore, it is possible that WS induces LRP1 mRNA expression and sLRP release by inhibiting intestinal BA reabsorption and consequent depletion in liver cell cholesterol. In addition, effective peripheral Aclearance by WS will depend on PM expression of liver LRP1 more than its mRNA expression. Hence, it is possible that WS treatment promotes LRP1 translocation to PM by improving insulin signaling and sensitivity. Aim 1: To determine whether treatment with WS inhibits intestinal BA reabsorption leading to reduced cell cholesterol and increased LRP1 expression in liver cells Aim 2: To determine whether treatment with WS improves insulin sensitivity and signalling leading to enhanced liver LRP1 PM expression and A uptake from plasma. ]]> Mon, 21 Jan 2013 18:48:21 GMT /slideshow/proposed-mechanism-underlying-the-therapeutic-effects-of-withania-somnifera-in-alzheimers-disease/16106254 TosifaMemon@slideshare.net(TosifaMemon) Proposed mechanism underlying the therapeutic effects of withania somnifera in alzheimers disease TosifaMemon I am Tosifa Memon, currently a phD candidate in Biology department at the University of Utah. I worked on this proposal for my qualifying exam and got the opportunity to present it to my thesis committee. Abstract: The root extract of Withania somnifera (WS), traditionally known to enhance memory, has been reported to improve cognitive and behavioral deficits in mice models of Alzheimers disease (AD). WS treatment was also found effective in reducing brain depositions and promoting peripheral clearance of toxic amyloid- (A) peptides which can otherwise interfere with normal neuronal function. How WS treatment exerts these beneficial effects remains unexplored and demands further investigation. Interestingly, Sehgal et al. study also found that WS treatment enhanced expression of liver low density lipoprotein-related protein (LRP1) along with plasma soluble form of LRP (sLRP), key players in peripheral A硫 clearance. Conversely, downregulation of liver LRP1 abrogated the therapeutic effects of WS extract and reduced plasma sLRP level. This finding not only highlights LRP1 as a potential target in AD treatment but also hints at WS components as potential leads for drug discovery. Therefore, it is imperative to know how treatment with WS root extract induces liver LRP1 expression. WS extract possesses hypocholesteremic and hypoglycemic activity. This may offer some explanation to therapeutic effects of WS treatment as abnormal cholesterol metabolism and insulin-resistance are known risk-factors in AD onset and progression. Like WS extract, cholesterol and insulin can also regulate LRP1 expression. Depletion in cell cholesterol, most likely by inhibiting bile acid (BA) reabsorption, can upregulate LRP1 mRNA expression and sLRP release while insulin stimulation promotes translocation of LRP1 from cytosol to plasma membrane (PM). Therefore, it is possible that WS induces LRP1 mRNA expression and sLRP release by inhibiting intestinal BA reabsorption and consequent depletion in liver cell cholesterol. In addition, effective peripheral Aclearance by WS will depend on PM expression of liver LRP1 more than its mRNA expression. Hence, it is possible that WS treatment promotes LRP1 translocation to PM by improving insulin signaling and sensitivity. Aim 1: To determine whether treatment with WS inhibits intestinal BA reabsorption leading to reduced cell cholesterol and increased LRP1 expression in liver cells Aim 2: To determine whether treatment with WS improves insulin sensitivity and signalling leading to enhanced liver LRP1 PM expression and A uptake from plasma. <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/proposedmechanismunderlyingthetherapeuticeffectsofwithaniasomniferainalzheimersdisease-130121184821-phpapp02-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> I am Tosifa Memon, currently a phD candidate in Biology department at the University of Utah. I worked on this proposal for my qualifying exam and got the opportunity to present it to my thesis committee. Abstract: The root extract of Withania somnifera (WS), traditionally known to enhance memory, has been reported to improve cognitive and behavioral deficits in mice models of Alzheimers disease (AD). WS treatment was also found effective in reducing brain depositions and promoting peripheral clearance of toxic amyloid- (A) peptides which can otherwise interfere with normal neuronal function. How WS treatment exerts these beneficial effects remains unexplored and demands further investigation. Interestingly, Sehgal et al. study also found that WS treatment enhanced expression of liver low density lipoprotein-related protein (LRP1) along with plasma soluble form of LRP (sLRP), key players in peripheral A硫 clearance. Conversely, downregulation of liver LRP1 abrogated the therapeutic effects of WS extract and reduced plasma sLRP level. This finding not only highlights LRP1 as a potential target in AD treatment but also hints at WS components as potential leads for drug discovery. Therefore, it is imperative to know how treatment with WS root extract induces liver LRP1 expression. WS extract possesses hypocholesteremic and hypoglycemic activity. This may offer some explanation to therapeutic effects of WS treatment as abnormal cholesterol metabolism and insulin-resistance are known risk-factors in AD onset and progression. Like WS extract, cholesterol and insulin can also regulate LRP1 expression. Depletion in cell cholesterol, most likely by inhibiting bile acid (BA) reabsorption, can upregulate LRP1 mRNA expression and sLRP release while insulin stimulation promotes translocation of LRP1 from cytosol to plasma membrane (PM). Therefore, it is possible that WS induces LRP1 mRNA expression and sLRP release by inhibiting intestinal BA reabsorption and consequent depletion in liver cell cholesterol. In addition, effective peripheral Aclearance by WS will depend on PM expression of liver LRP1 more than its mRNA expression. Hence, it is possible that WS treatment promotes LRP1 translocation to PM by improving insulin signaling and sensitivity. Aim 1: To determine whether treatment with WS inhibits intestinal BA reabsorption leading to reduced cell cholesterol and increased LRP1 expression in liver cells Aim 2: To determine whether treatment with WS improves insulin sensitivity and signalling leading to enhanced liver LRP1 PM expression and A uptake from plasma.
Proposed mechanism underlying the therapeutic effects of withania somnifera in alzheimers disease from Tosifa Memon
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