While we wait .... Probably mentioned this befo
Post# of 148171
Probably mentioned this before, but I am very interested in the memory application of VX. My wife does not take it lightly when I explain that I called her by a different name because of my memory causing me few “near misses” to the ICU .
Posted some remarks about this some time back, however Dr. Patterson (via twitter) and somebody else in this board (sorry, forgot who posted it) highlighted this article: “The Chemokine MIP-1α/CCL3 impairs mouse hippocampal synaptic transmission, plasticity and memory” .
https://www.researchgate.net/publication/2833...and_memory
This relates to us because CCL3 binds to our receptor CCR5, so our antagonist will have direct effect in this findings which indeed is what the researchers conclude (they even used Maraviroc):
Quote:
Importantly, our in vivo data demonstrate that detrimental effects of CCL3 upon synaptic transmission and plasticity were also observed in hippocampal slices from animals sub-chronically injected with CCL3 in ventricles. The detrimental effect of CCL3 appears mediated by CCR5 receptor, as it was reversed by the specific antagonist Maraviroc. CCR5 is one of the cognate CCL3 receptor previously reported to be expressed by astrocytes, microglia and neurons. Our data extend the known neuromodulatory role of the CCR5 receptor. Indeed, CCR5 was found to enhance pain perception at inflammatory sites and to modulate glutamate release in human neocortex
And:
Quote:
In line with the latter studies, blockade of CCR5 by Maraviroc impacts plasticity and memory only in the presence of CCL3 without any effect by itself, finally suggesting that the tonic CCR5 activity is not necessary to memory formation in non-pathological conditions. Altogether, our data highlight for the first time that abnormal activation of the CCR5 pathway is prone to impair synaptic processes leading to memory loss, supporting a role in pathologies associated with CCL3 upsurge.
Another proof (as if we needed more) is that a high percentage of individuals with true photographic memory, Hyperthymesia (or photographic memory) are homozygous for the deletion variant of the ccr5 gene.
I attach below for completeness cut-and-paste from my former post in regards to this matter. Once VX is available I might try to get some to improve my memory & avoid risking my life with my wife.
There have been some reports of CCR5 being associated with much improved memory (Hyperthymesia), and reports of the CRISP-edited Chinese girls that where given the gene mutation was really to improve their performance.
https://biohackinfo.com/news-crispr-babies-cc...-immunity/
Some scientific experiments with rats indeed have indeed demonstrated that CCR5 is a suppressor for cortical plasticity and hippocampal learning and memory. This was discovered on a reverse genetic memory screen. Basically, some mice with heterozygous deletion of CCR5 performed much better than other mice.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5213777/
Their conclusion: CCR5 overexpression leads to learning and memory deficits (we are talking mice here).
However, there exist HAND or HIV-associated neurocognitive disorders which remain a chronic issue, with significant effects on patients ability to perform activities of daily living, quality of life, employment, medication adherence, and survival.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5365228/
CCR5 chemokine receptor neurotropism has been identified as a biomarker of this CNS (central nervous system) disorder.
Quote:
CCR5 chemokine receptor neurotropism Viral envelope glycoproteins can fuse with only those cells expressing both CD4 and an HIV co-receptor, of which CCR5 has been identified as the most important for microglia and CNS macrophages. CCR5 receptors are upregulated on activated CD4+ and CD8+ T cells, enhancing antigen-presenting cell interaction, T cell trafficking into tissues, and cytokine production. In response to infection or inflammation, monocytes, microglia, astrocytes, and neurons express CCR5 ligands, which increase the migration of CCR5+ T cells into the CNS. Locally, these effector T cells secrete CCR5 ligands, which amplify the immune response. A subset of CCR5-tropic viruses have been found to be highly fusogenic, requiring lower expression levels of CCR5 and CD4 to infect cells, leading to greater apoptosis. There is now good evidence that the vast majority of HIV strains in the brain are CCR5 tropic. Given the intrinsic role of CCR5 in CNS disease, it is suggested that CCR5 antagonists, such as maraviroc, may be able to reduce the migration and then activation of effector CD8+ T cells in the CNS and hence reduce the neurocognitive sequelae of HIV. This is now being assessed
Quote:
A recent prospective, open-label pilot randomized controlled trial in individuals with viral suppression and stable ART for 12 months found maraviroc-intensified HAART improved global neurocognitive performance at both 6 and 12 months without significant side effects
So, it seems that VX (Leronlimab) WILL help with HAND and improves cognition and memory !!!
Perhaps OHM would add to his list two more indications for Vyrologix:
1) Stupidity
2) Bad memory
I am suffering of a mild case of one and critical of the other.