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The relationship between unprotected sex, brain damage, and the thousand cock stare
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<blockquote data-quote="rawhide" data-source="post: 564722" data-attributes="member: 3648"><p>At this point, the original post is more science fiction than anything else. It's so ridiculous I can't believe you guys are fixated on it. Seriously, more than a century of human blood transfusions not to mention organ transplants. Hemophiliacs should be pretty fucked up with zombie eyes if that were the case.</p><p></p><p>On the other hand, here's this backing up what I said early relating to "Mommy Brain."</p><p></p><p>1. Endocrinology. 2010 Nov;151(11):5380-8. doi: 10.1210/en.2009-1168. Epub 2010 Sep 15.</p><p>Effect of chronic hCG administration on Alzheimer's-related cognition and A beta accumulation in PS1KI mice.</p><p>Barron AM1, Verdile G, Taddei K, Bates KA, Martins RN.</p><p>Author information: </p><p>1School of Psychiatry and Clinical Neurosciences, The University of Western Australia, Nedlands, 6009, Australia.</p><p></p><p>Abstract</p><p>Age-associated changes in the reproductive hormones-the gonadal steroid hormones and the gonadotropins-have been identified as potential risk factors for Alzheimer's disease (AD). However, levels of gonadotropins and estrogens are closely linked in vivo, and it has proven difficult to separate the effects of gonadotropins from the well-documented estrogenic effects on AD-related neuropathology in experimental models of menopause. To assess the effects of gonadotropins on cognition and AD biochemical markers independent of estrogenic effects, a potent analog of luteinizing hormone [human chorionic gonadotropin (hCG)] was administered to ovariectomized presenilin1 knock-in mice (PS1KI). Gonadotropin administration was found to induce hyperactivity and anxiety (Open Field Maze and Taste Neophobia Task) and working memory dysfunction, without altering reference memory (Morris Water Maze). Although gonadotropin administration modestly altered β amyloid (Aβ40) levels, levels of the longer more toxic form (Aβ42) were unaffected. Furthermore, altered Aβ40 levels were not associated with observed behavioral and cognitive impairments. <strong>These findings provide proof, in principle, that the gonadotropin hormones play a role in the modulation of AD-related behavior, cognition, and neuropathology.</strong></p><p> PMID: 20844010 [PubMed - indexed for MEDLINE] </p><p> Icon for Atypon </p><p> </p><p></p><p>1. Cell Mol Neurobiol. 2013 Aug;33(6):747-51. doi: 10.1007/s10571-013-9954-3. Epub 2013 Jun 28.</p><p>Human chorionic gonadotropin increases β-cleavage of amyloid precursor protein in SH-SY5Y cells.</p><p>Saberi S1, Du YP, Christie M, Goldsbury C.</p><p>Author information: </p><p>1Brain and Mind Research Institute, School of Medical Sciences, University of Sydney, Sydney, NSW, Australia.</p><p></p><p>Abstract</p><p><strong>Elevated levels of amyloid-β (Aβ) peptides, the main component of amyloid plaques in Alzheimer's disease, are the result of excessive β- and γ-cleavage of the amyloid precursor protein (APP) and/or impaired Aβ clearance in the brain. It has been suggested that high concentrations of luteinizing hormone (LH) in women contribute to increased Aβ generation after menopause, but the mechanism for this is incompletely understood. We investigated the effect of human chorionic gonadotropin (hCG), an LH receptor agonist, on APP β-cleavage in the SH-SY5Y neuroblastoma cell line. Treatment of these cells with hCG-induced elevated β-cleavage in a dose-dependent manner: administration of 30 mIU but not 10 mIU/ml of hCG significantly increased sAPPβ levels in the cell medium 1.7-fold as measured by ELISA. These results support the notion that LH contributes to elevated Aβ levels at least in part by increasing β-cleavage of APP by β-site APP cleaving enzyme.</strong></p><p> <strong></strong></p><p> PMID: 23812658 [PubMed - indexed for MEDLINE</p></blockquote><p></p>
[QUOTE="rawhide, post: 564722, member: 3648"] At this point, the original post is more science fiction than anything else. It's so ridiculous I can't believe you guys are fixated on it. Seriously, more than a century of human blood transfusions not to mention organ transplants. Hemophiliacs should be pretty fucked up with zombie eyes if that were the case. On the other hand, here's this backing up what I said early relating to "Mommy Brain." 1. Endocrinology. 2010 Nov;151(11):5380-8. doi: 10.1210/en.2009-1168. Epub 2010 Sep 15. Effect of chronic hCG administration on Alzheimer's-related cognition and A beta accumulation in PS1KI mice. Barron AM1, Verdile G, Taddei K, Bates KA, Martins RN. Author information: 1School of Psychiatry and Clinical Neurosciences, The University of Western Australia, Nedlands, 6009, Australia. Abstract Age-associated changes in the reproductive hormones-the gonadal steroid hormones and the gonadotropins-have been identified as potential risk factors for Alzheimer's disease (AD). However, levels of gonadotropins and estrogens are closely linked in vivo, and it has proven difficult to separate the effects of gonadotropins from the well-documented estrogenic effects on AD-related neuropathology in experimental models of menopause. To assess the effects of gonadotropins on cognition and AD biochemical markers independent of estrogenic effects, a potent analog of luteinizing hormone [human chorionic gonadotropin (hCG)] was administered to ovariectomized presenilin1 knock-in mice (PS1KI). Gonadotropin administration was found to induce hyperactivity and anxiety (Open Field Maze and Taste Neophobia Task) and working memory dysfunction, without altering reference memory (Morris Water Maze). Although gonadotropin administration modestly altered β amyloid (Aβ40) levels, levels of the longer more toxic form (Aβ42) were unaffected. Furthermore, altered Aβ40 levels were not associated with observed behavioral and cognitive impairments. [b]These findings provide proof, in principle, that the gonadotropin hormones play a role in the modulation of AD-related behavior, cognition, and neuropathology.[/b] PMID: 20844010 [PubMed - indexed for MEDLINE] Icon for Atypon 1. Cell Mol Neurobiol. 2013 Aug;33(6):747-51. doi: 10.1007/s10571-013-9954-3. Epub 2013 Jun 28. Human chorionic gonadotropin increases β-cleavage of amyloid precursor protein in SH-SY5Y cells. Saberi S1, Du YP, Christie M, Goldsbury C. Author information: 1Brain and Mind Research Institute, School of Medical Sciences, University of Sydney, Sydney, NSW, Australia. Abstract [b]Elevated levels of amyloid-β (Aβ) peptides, the main component of amyloid plaques in Alzheimer's disease, are the result of excessive β- and γ-cleavage of the amyloid precursor protein (APP) and/or impaired Aβ clearance in the brain. It has been suggested that high concentrations of luteinizing hormone (LH) in women contribute to increased Aβ generation after menopause, but the mechanism for this is incompletely understood. We investigated the effect of human chorionic gonadotropin (hCG), an LH receptor agonist, on APP β-cleavage in the SH-SY5Y neuroblastoma cell line. Treatment of these cells with hCG-induced elevated β-cleavage in a dose-dependent manner: administration of 30 mIU but not 10 mIU/ml of hCG significantly increased sAPPβ levels in the cell medium 1.7-fold as measured by ELISA. These results support the notion that LH contributes to elevated Aβ levels at least in part by increasing β-cleavage of APP by β-site APP cleaving enzyme. [/b] PMID: 23812658 [PubMed - indexed for MEDLINE [/QUOTE]
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