Dear longs,

We are in the presence of a "miracle" molecule. But let's talk about memory. It has been demonstrated in several studies that CCR5 is involved in the memory
processing/retention chain and also in recovery after traumatic brain injury:

CCR5 Is a Therapeutic Target for Recovery after Stroke and Traumatic Brain Injury

https://www.sciencedirect.com/science/article...7419301072

Quote:

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Summary
We tested a newly described molecular memory system, CCR5 signaling, for its role in recovery after stroke and traumatic brain injury (TBI). CCR5 is uniquely expressed in cortical neurons after stroke. Post-stroke neuronal knockdown of CCR5 in pre-motor cortex leads to early recovery of motor control. Recovery is associated with preservation of dendritic spines, new patterns of cortical projections to contralateral pre-motor cortex, and upregulation of CREB and DLK signaling. Administration of a clinically utilized FDA-approved CCR5 antagonist, devised for HIV treatment, produces similar effects on motor recovery post stroke and cognitive decline post TBI. Finally, in a large clinical cohort of stroke patients, carriers for a naturally occurring loss-of-function mutation in CCR5 (CCR5-?32) exhibited greater recovery of neurological impairments and cognitive function. In summary, CCR5 is a translational target for neural repair in stroke and TBI and the first reported gene associated with enhanced recovery in human stroke.

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Also in:

Insight into the roles of CCR5 in learning and memory in normal and disordered states

https://pubmed.ncbi.nlm.nih.gov/33276089/

Quote:

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Abstract
As cognitive impairments continue to rise in prevalence, there is an urgent need to understand the mechanisms of learning and memory in normal and disordered states. C-C chemokine receptor 5 (CCR5) has been implicated in the regulation of multiple forms of learning and memory via its regulation on learning-related cell signaling and neuronal plasticity. As a chemokine receptor and a co-receptor for HIV, CCR5's role in immune response and HIV-associated neurocognitive disorder (HAND) has been widely studied. In contrast, CCR5 is less understood in cognitive deficits associated with other disorders, including Alzheimer's disease (AD), stroke and certain psychiatric disorders. A broad overview of the present literature shows that CCR5 acts as a potent suppressor of synaptic plasticity and learning and memory, although a few studies have reported the opposite effect of CCR5 in stroke or AD animal models. By summarizing the current literature of CCR5 in animal and human studies of cognition, this review aims to provide a comprehensive overview of the role of CCR5 in learning and memory in both normal and disordered states and to discuss the possibility of CCR5 suppression as an effective therapeutic to alleviate cognitive deficits in HAND, AD, and stroke.

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Also:

CCR5 closes the temporal window for memory linking

https://www.nature.com/articles/s41586-022-04783-1

Quote:

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Abstract
Real-world memories are formed in a particular context and are often not acquired or recalled in isolation. Time is a key variable in the organization of memories, as events that are experienced close in time are more likely to be meaningfully associated, whereas those that are experienced with a longer interval are not. How the brain segregates events that are temporally distinct is unclear. Here we show that a delayed (12–24 h) increase in the expression of C-C chemokine receptor type 5 (CCR5)—an immune receptor that is well known as a co-receptor for HIV infection—after the formation of a contextual memory determines the duration of the temporal window for associating or linking that memory with subsequent memories. This delayed expression of CCR5 in mouse dorsal CA1 neurons results in a decrease in neuronal excitability, which in turn negatively regulates neuronal memory allocation, thus reducing the overlap between dorsal CA1 memory ensembles. Lowering this overlap affects the ability of one memory to trigger the recall of the other, and therefore closes the temporal window for memory linking. Our findings also show that an age-related increase in the neuronal expression of CCR5 and its ligand CCL5 leads to impairments in memory linking in aged mice, which could be reversed with a Ccr5 knockout and a drug approved by the US Food and Drug Administration (FDA) that inhibits this receptor, a result with clinical implications. Altogether, the findings reported here provide insights into the molecular and cellular mechanisms that shape the temporal window for memory linking.

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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/

And, In fact, it's estimated that ~10 percent of individuals with true photographic memory are homozygous for the deletion variant of the CCR5 gene.

So, if we had our act together, we should be pursuing this venue (and others), however this application alone would mean several "fingers" in the SP.

Yeah ... maybe we should be all "shooting" Leronlimab

You all have a wonderful Holiday season ... lets hope that Father Christmas brings a nicely wrapped letter saying: "congratulations , you have been a good boy all year: the hold is therefore lifted !!!"