Guest guest Posted May 4, 2010 Report Share Posted May 4, 2010 Thank you for that information. It helps make better decisions when you are better informed! From: [mailto: ] On Behalf Of ElyseG Sent: May-04-10 5:16 PM Subject: SSRI's v alternative While I am sure some believe you can do this with natural stuff you can NOT it has never changed a spect scan SSRI's are found to be neuroprotective Elyse Goldberg J Neurosci Res. 2009 Mar;87(4):1037-45. Fluoxetine affords robust neuroprotection in the postischemic brain via its anti-inflammatory effect. Lim CM, Kim SW, Park JY, Kim C, Yoon SH, Lee JK. Department of Anatomy, Inha University School of Medicine, Inchon, Korea. Abstract Fluoxetine is a selective serotonin reuptake inhibitor that is widely used in the treatment of major depression including after stroke. In this study, we tested whether fluoxetine protects neuronal death in a rat cerebral ischemia model of middle cerebral artery occlusion (MCAO). The administration of fluoxetine intravenously (10 mg/kg) at 30 min, 3 hr, or 6 hr after MCAO reduced infarct volumes to 21.2+/-6.7%, 14.5+/-3.0%, and 22.8+/-2.9%, respectively, of that of the untreated control. Moreover, the neuroprotective effect of fluoxetine was evident when it was administered as late as 9 hr after MCAO/reperfusion. These neuroprotective effects were accompanied by improvement of motor impairment and neurological deficits. The fluoxetine-treated brain was found to show marked repressions of microglia activation, neutrophil infiltration, and proinflammatory marker expressions. Moreover, fluoxetine suppressed NF-kappaB activity dose-dependently in the postischemic brain and also in lipopolysaccharide-treated primary microglia and neutrophil cultures, suggesting that NF-kappaB activity inhibition explains in part its anti-inflammatory effect. These results demonstrate that curative treatment of fluoxetine affords strong protection against delayed cerebral ischemic injury, and that these neuroprotective effects might be associated with its anti-inflammatory effects. PMID: 18855941 [PubMed - indexed for MEDLINE] Publication Types, MeSH Terms, Substances Neurobiol Dis. 2008 Jun;30(3):312-22. Epub 2008 Mar 10. Sertraline slows disease progression and increases neurogenesis in N171-82Q mouse model of Huntington's disease. Duan W, Peng Q, Masuda N, Ford E, Tryggestad E, Ladenheim B, Zhao M, Cadet JL, Wong J, Ross CA. Division of Neurobiology, Department of Psychiatry and Behavioral Sciences, s Hopkins University School of Medicine, CMSC 8-121, 600 North Wolfe Street, Baltimore, MD 21287, USA. wduan2@... <mailto:wduan2%40jhmi.edu> Abstract Huntington's disease (HD) is an inherited progressive neurodegenerative disorder resulting from CAG repeat expansion in the gene that encodes for the protein huntingtin. To identify neuroprotective compound (s) that can slow down disease progression and can be administered long term with few side effects in Huntington's disease, we investigated the effect of sertraline, a selective serotonin reuptake inhibitor (SSRI) which has been shown to upregulate BDNF levels in rodent brains. We report here that in HD mice sertraline increased BDNF levels, preserved chaperone protein HSP70 and Bcl-2 levels in brains, attenuated the progression of brain atrophy and behavioral abnormalities and thereby increased survival. Sertraline also enhanced neurogenesis, which appeared to be responsible for mediating the beneficial effects of sertraline in HD mice. Additionally, the effective levels of sertraline are comparable to the safe levels achievable in humans. The findings suggest that sertraline is a potential candidate for treatment of HD patients. PMID: 18403212 [PubMed - indexed for MEDLINE] Brain Res. 2009 Jul 24;1281:108-16. Epub 2009 May 7. Fluoxetine attenuates kainic acid-induced neuronal cell death in the mouse hippocampus. Jin Y, Lim CM, Kim SW, Park JY, Seo JS, Han PL, Yoon SH, Lee JK. Department of Anatomy and Center for Advanced Medical Education (BK21 project), Inha University School of Medicine, Incheon, Republic of Korea. Abstract Fluoxetine is a selective serotonin reuptake inhibitor (SSRI) and one of the commonly prescribed antidepressants. Numerous clinical observations and animal studies indicate that fluoxetine enhances the anticonvulsant potencies of several antiepileptic drugs. In the previous report, we showed that fluoxetine strongly protects against delayed cerebral ischemic injury. In the present study, the authors investigated whether fluoxetine has a beneficial effect on KA-induced neuronal cell death. An intracerebroventricular (i.c.v.) injection of 0.94 nmol (0.2 microg) of KA produced typical neuronal cell death both in CA1 and CA3 regions of the hippocampus. Although, there was no significant difference in the time course or severity of epileptic behavior, the systemic administration of fluoxetine 30 min before KA administration significantly attenuated this neuronal cell death. Fluoxetine was found to suppress neuronal cell loss when injected at 10 mg/kg and the effect was enhanced at 50 mg/kg. Furthermore, this fluoxetine-induced neuroprotection was accompanied by marked improvements in memory impairment, as determined by passive avoidance tests. KA-induced gliosis and proinflammatory marker (COX-2, IL-1beta, and TNF-alpha) inductions were also suppressed by fluoxetine administration. It is interesting to note here that fluoxetine treatment suppressed NF-kappaB activity dose-dependently in KA-treated mouse brains, suggesting that this explains in part its anti-inflammatory effect. Together, these results suggest that fluoxetine has therapeutic potential in terms of suppressing KA-induced pathogenesis in the brain, and that these neuroprotective effects are associated with its anti-inflammatory effects. PMID: 19427844 [PubMed - indexed for MEDLINE] Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 4, 2010 Report Share Posted May 4, 2010 Does anyone know the effects of low low dose risperidone on SPECT scans? From: [mailto: ] On Behalf Of and Freeman Sent: May-04-10 6:48 PM Subject: RE: SSRI's v alternative Thank you for that information. It helps make better decisions when you are better informed! From: <mailto:%40> [mailto: <mailto:%40> ] On Behalf Of ElyseG Sent: May-04-10 5:16 PM <mailto:%40> Subject: SSRI's v alternative While I am sure some believe you can do this with natural stuff you can NOT it has never changed a spect scan SSRI's are found to be neuroprotective Elyse Goldberg J Neurosci Res. 2009 Mar;87(4):1037-45. Fluoxetine affords robust neuroprotection in the postischemic brain via its anti-inflammatory effect. Lim CM, Kim SW, Park JY, Kim C, Yoon SH, Lee JK. Department of Anatomy, Inha University School of Medicine, Inchon, Korea. Abstract Fluoxetine is a selective serotonin reuptake inhibitor that is widely used in the treatment of major depression including after stroke. In this study, we tested whether fluoxetine protects neuronal death in a rat cerebral ischemia model of middle cerebral artery occlusion (MCAO). The administration of fluoxetine intravenously (10 mg/kg) at 30 min, 3 hr, or 6 hr after MCAO reduced infarct volumes to 21.2+/-6.7%, 14.5+/-3.0%, and 22.8+/-2.9%, respectively, of that of the untreated control. Moreover, the neuroprotective effect of fluoxetine was evident when it was administered as late as 9 hr after MCAO/reperfusion. These neuroprotective effects were accompanied by improvement of motor impairment and neurological deficits. The fluoxetine-treated brain was found to show marked repressions of microglia activation, neutrophil infiltration, and proinflammatory marker expressions. Moreover, fluoxetine suppressed NF-kappaB activity dose-dependently in the postischemic brain and also in lipopolysaccharide-treated primary microglia and neutrophil cultures, suggesting that NF-kappaB activity inhibition explains in part its anti-inflammatory effect. These results demonstrate that curative treatment of fluoxetine affords strong protection against delayed cerebral ischemic injury, and that these neuroprotective effects might be associated with its anti-inflammatory effects. PMID: 18855941 [PubMed - indexed for MEDLINE] Publication Types, MeSH Terms, Substances Neurobiol Dis. 2008 Jun;30(3):312-22. Epub 2008 Mar 10. Sertraline slows disease progression and increases neurogenesis in N171-82Q mouse model of Huntington's disease. Duan W, Peng Q, Masuda N, Ford E, Tryggestad E, Ladenheim B, Zhao M, Cadet JL, Wong J, Ross CA. Division of Neurobiology, Department of Psychiatry and Behavioral Sciences, s Hopkins University School of Medicine, CMSC 8-121, 600 North Wolfe Street, Baltimore, MD 21287, USA. wduan2@... <mailto:wduan2%40jhmi.edu> <mailto:wduan2%40jhmi.edu> Abstract Huntington's disease (HD) is an inherited progressive neurodegenerative disorder resulting from CAG repeat expansion in the gene that encodes for the protein huntingtin. To identify neuroprotective compound (s) that can slow down disease progression and can be administered long term with few side effects in Huntington's disease, we investigated the effect of sertraline, a selective serotonin reuptake inhibitor (SSRI) which has been shown to upregulate BDNF levels in rodent brains. We report here that in HD mice sertraline increased BDNF levels, preserved chaperone protein HSP70 and Bcl-2 levels in brains, attenuated the progression of brain atrophy and behavioral abnormalities and thereby increased survival. Sertraline also enhanced neurogenesis, which appeared to be responsible for mediating the beneficial effects of sertraline in HD mice. Additionally, the effective levels of sertraline are comparable to the safe levels achievable in humans. The findings suggest that sertraline is a potential candidate for treatment of HD patients. PMID: 18403212 [PubMed - indexed for MEDLINE] Brain Res. 2009 Jul 24;1281:108-16. Epub 2009 May 7. Fluoxetine attenuates kainic acid-induced neuronal cell death in the mouse hippocampus. Jin Y, Lim CM, Kim SW, Park JY, Seo JS, Han PL, Yoon SH, Lee JK. Department of Anatomy and Center for Advanced Medical Education (BK21 project), Inha University School of Medicine, Incheon, Republic of Korea. Abstract Fluoxetine is a selective serotonin reuptake inhibitor (SSRI) and one of the commonly prescribed antidepressants. Numerous clinical observations and animal studies indicate that fluoxetine enhances the anticonvulsant potencies of several antiepileptic drugs. In the previous report, we showed that fluoxetine strongly protects against delayed cerebral ischemic injury. In the present study, the authors investigated whether fluoxetine has a beneficial effect on KA-induced neuronal cell death. An intracerebroventricular (i.c.v.) injection of 0.94 nmol (0.2 microg) of KA produced typical neuronal cell death both in CA1 and CA3 regions of the hippocampus. Although, there was no significant difference in the time course or severity of epileptic behavior, the systemic administration of fluoxetine 30 min before KA administration significantly attenuated this neuronal cell death. Fluoxetine was found to suppress neuronal cell loss when injected at 10 mg/kg and the effect was enhanced at 50 mg/kg. Furthermore, this fluoxetine-induced neuroprotection was accompanied by marked improvements in memory impairment, as determined by passive avoidance tests. KA-induced gliosis and proinflammatory marker (COX-2, IL-1beta, and TNF-alpha) inductions were also suppressed by fluoxetine administration. It is interesting to note here that fluoxetine treatment suppressed NF-kappaB activity dose-dependently in KA-treated mouse brains, suggesting that this explains in part its anti-inflammatory effect. Together, these results suggest that fluoxetine has therapeutic potential in terms of suppressing KA-induced pathogenesis in the brain, and that these neuroprotective effects are associated with its anti-inflammatory effects. PMID: 19427844 [PubMed - indexed for MEDLINE] Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 5, 2010 Report Share Posted May 5, 2010 I dont know how it would effect a scan, but my son took Risperadal for a year. It is an antipsychotic. My doctor prescribed it because it is approved to treat aggression in autism. It sedated my son, made it harder for him to talk, and he fell asleep at school sometimes. When I finally took him off it, there was really no change in his behavior. His aggression had really been about adjusting to a new school and PANDAS. Once he had adjusted, an was no longer ticking, he had not been aggressive. I have taken Lexapro to deal with depression and anxiety. It works wonders for me. Does anyone know if Lexapro is helpful with autism? > > Does anyone know the effects of low low dose risperidone on SPECT scans? > > > > From: [mailto: ] On Behalf Of > and Freeman > Sent: May-04-10 6:48 PM > > Subject: RE: SSRI's v alternative > > > > > > Thank you for that information. It helps make better decisions when you are > better informed! > > > > From: <mailto:%40> > [mailto: <mailto:%40> ] On Behalf Of > ElyseG > Sent: May-04-10 5:16 PM > <mailto:%40> > Subject: SSRI's v alternative > > While I am sure some believe you can do this with natural stuff you can NOT > it has never changed a spect scan > > SSRI's are found to be neuroprotective > > Elyse Goldberg > > J Neurosci Res. 2009 Mar;87(4):1037-45. > Fluoxetine affords robust neuroprotection in the postischemic brain via its > anti-inflammatory effect. > Lim CM, Kim SW, Park JY, Kim C, Yoon SH, Lee JK. > Department of Anatomy, Inha University School of Medicine, Inchon, Korea. > Abstract > Fluoxetine is a selective serotonin reuptake inhibitor that is widely used > in the treatment of major depression including after stroke. In this study, > we tested whether fluoxetine protects neuronal death in a rat cerebral > ischemia model of middle cerebral artery occlusion (MCAO). The > administration of fluoxetine intravenously (10 mg/kg) at 30 min, 3 hr, or 6 > hr after MCAO reduced infarct volumes to 21.2+/-6.7%, 14.5+/-3.0%, and > 22.8+/-2.9%, respectively, of that of the untreated control. Moreover, the > neuroprotective effect of fluoxetine was evident when it was administered as > late as 9 hr after MCAO/reperfusion. These neuroprotective effects were > accompanied by improvement of motor impairment and neurological deficits. > The fluoxetine-treated brain was found to show marked repressions of > microglia activation, neutrophil infiltration, and proinflammatory marker > expressions. Moreover, fluoxetine suppressed NF-kappaB activity > dose-dependently in the postischemic brain and also in > lipopolysaccharide-treated primary microglia and neutrophil cultures, > suggesting that NF-kappaB activity inhibition explains in part its > anti-inflammatory effect. These results demonstrate that curative treatment > of fluoxetine affords strong protection against delayed cerebral ischemic > injury, and that these neuroprotective effects might be associated with its > anti-inflammatory effects. > PMID: 18855941 [PubMed - indexed for MEDLINE] > Publication Types, MeSH Terms, Substances > > Neurobiol Dis. 2008 Jun;30(3):312-22. Epub 2008 Mar 10. > Sertraline slows disease progression and increases neurogenesis in N171-82Q > mouse model of Huntington's disease. > Duan W, Peng Q, Masuda N, Ford E, Tryggestad E, Ladenheim B, Zhao M, Cadet > JL, Wong J, Ross CA. > Division of Neurobiology, Department of Psychiatry and Behavioral Sciences, > s Hopkins University School of Medicine, CMSC 8-121, 600 North Wolfe > Street, Baltimore, MD 21287, USA. wduan2@... <mailto:wduan2%40jhmi.edu> > <mailto:wduan2%40jhmi.edu> > > Abstract > Huntington's disease (HD) is an inherited progressive neurodegenerative > disorder resulting from CAG repeat expansion in the gene that encodes for > the protein huntingtin. To identify neuroprotective compound (s) that can > slow down disease progression and can be administered long term with few > side effects in Huntington's disease, we investigated the effect of > sertraline, a selective serotonin reuptake inhibitor (SSRI) which has been > shown to upregulate BDNF levels in rodent brains. We report here that in HD > mice sertraline increased BDNF levels, preserved chaperone protein HSP70 and > Bcl-2 levels in brains, attenuated the progression of brain atrophy and > behavioral abnormalities and thereby increased survival. Sertraline also > enhanced neurogenesis, which appeared to be responsible for mediating the > beneficial effects of sertraline in HD mice. Additionally, the effective > levels of sertraline are comparable to the safe levels achievable in humans. > The findings suggest that sertraline is a potential candidate for treatment > of HD patients. > PMID: 18403212 [PubMed - indexed for MEDLINE] > Brain Res. 2009 Jul 24;1281:108-16. Epub 2009 May 7. > Fluoxetine attenuates kainic acid-induced neuronal cell death in the mouse > hippocampus. > Jin Y, Lim CM, Kim SW, Park JY, Seo JS, Han PL, Yoon SH, Lee JK. > Department of Anatomy and Center for Advanced Medical Education (BK21 > project), Inha University School of Medicine, Incheon, Republic of Korea. > Abstract > Fluoxetine is a selective serotonin reuptake inhibitor (SSRI) and one of the > commonly prescribed antidepressants. Numerous clinical observations and > animal studies indicate that fluoxetine enhances the anticonvulsant > potencies of several antiepileptic drugs. In the previous report, we showed > that fluoxetine strongly protects against delayed cerebral ischemic injury. > In the present study, the authors investigated whether fluoxetine has a > beneficial effect on KA-induced neuronal cell death. An > intracerebroventricular (i.c.v.) injection of 0.94 nmol (0.2 microg) of KA > produced typical neuronal cell death both in CA1 and CA3 regions of the > hippocampus. Although, there was no significant difference in the time > course or severity of epileptic behavior, the systemic administration of > fluoxetine 30 min before KA administration significantly attenuated this > neuronal cell death. Fluoxetine was found to suppress neuronal cell loss > when injected at 10 mg/kg and the effect was enhanced at 50 mg/kg. > Furthermore, this fluoxetine-induced neuroprotection was accompanied by > marked improvements in memory impairment, as determined by passive avoidance > tests. KA-induced gliosis and proinflammatory marker (COX-2, IL-1beta, and > TNF-alpha) inductions were also suppressed by fluoxetine administration. It > is interesting to note here that fluoxetine treatment suppressed NF-kappaB > activity dose-dependently in KA-treated mouse brains, suggesting that this > explains in part its anti-inflammatory effect. Together, these results > suggest that fluoxetine has therapeutic potential in terms of suppressing > KA-induced pathogenesis in the brain, and that these neuroprotective effects > are associated with its anti-inflammatory effects. > PMID: 19427844 [PubMed - indexed for MEDLINE] > > Quote Link to comment Share on other sites More sharing options...
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