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HCG and elevated LH in Alzheimer patients
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<blockquote data-quote="Cataceous" data-source="post: 244438" data-attributes="member: 38109"><p>Interesting. They hypothesize that excess hCG/LH downregulates the LH receptors in the brain, leading to the cognitive issues. After seeing all this I would more than ever steer guys away from hCG monotherapy and encourage use of the lowest effective dose with TRT. There could also be ramifications for guys using SERMs—perhaps they should ensure LH remains physiological.</p><p></p><p style="margin-left: 20px"><em>... To this end, it well understood that that LHCGR is quickly internalized and downregulated in the presence of high levels of its ligand (Peegel et al., 1994). Thus, under the hypothesis that LH crosses the blood brain barrier to bind LHCGR, <strong>high levels of LH within the brain could downregulate LHCGR expression and lead to cognitive deficits</strong>. Reducing circulating LH with GnRHR antagonists could in turn allow LHCGR levels to normalize and resume its normal function. Alternatively, one could also speculate that supra-physiological levels of LH or hCG delivered directly into the brain or delivered to gonadectomized animals (already with high levels of circulating LH) could have similar downregulating effects onto LHCGR expression, which could also impact signaling and function negatively. This would explain why studies using high doses of hCG (Barron et al., 2010; Lukacs et al., 1995) would have detrimental effects on function but studies using lower doses (Blair et al., 2019; Movsas et al., 2017) would have beneficial effects. Thus, precisely characterizing central LHCGR dynamics under different treatment conditions seems to be imperative to understand the nature of the effects of this hormone and its receptor's potential as a therapeutic target for age-related neurodegenerative disease such as AD.</em></p></blockquote><p></p>
[QUOTE="Cataceous, post: 244438, member: 38109"] Interesting. They hypothesize that excess hCG/LH downregulates the LH receptors in the brain, leading to the cognitive issues. After seeing all this I would more than ever steer guys away from hCG monotherapy and encourage use of the lowest effective dose with TRT. There could also be ramifications for guys using SERMs—perhaps they should ensure LH remains physiological. [INDENT][I]... To this end, it well understood that that LHCGR is quickly internalized and downregulated in the presence of high levels of its ligand (Peegel et al., 1994). Thus, under the hypothesis that LH crosses the blood brain barrier to bind LHCGR, [B]high levels of LH within the brain could downregulate LHCGR expression and lead to cognitive deficits[/B]. Reducing circulating LH with GnRHR antagonists could in turn allow LHCGR levels to normalize and resume its normal function. Alternatively, one could also speculate that supra-physiological levels of LH or hCG delivered directly into the brain or delivered to gonadectomized animals (already with high levels of circulating LH) could have similar downregulating effects onto LHCGR expression, which could also impact signaling and function negatively. This would explain why studies using high doses of hCG (Barron et al., 2010; Lukacs et al., 1995) would have detrimental effects on function but studies using lower doses (Blair et al., 2019; Movsas et al., 2017) would have beneficial effects. Thus, precisely characterizing central LHCGR dynamics under different treatment conditions seems to be imperative to understand the nature of the effects of this hormone and its receptor's potential as a therapeutic target for age-related neurodegenerative disease such as AD.[/I][/INDENT] [/QUOTE]
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HCG and elevated LH in Alzheimer patients
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