Ohm, I'm glad you mentioned CCL11. After some
Post# of 155045
(Total Views: 578)
Posted On: 11/22/2021 7:20:42 PM
Ohm,
I'm glad you mentioned CCL11. After some of the memory implications I was taking a look at over the weekend, I wanted to search CCR5 in CTE (chronic traumatic enchephalopathy) - largely as a follow up to a theory Ive been kicking around concerning inflammation in PTSD, concussions, depression, and others. Since Leronlimab down-regulates CCL11, perhaps we can have a positive effect for those suffering from CTE, or other brain affected inflammatory disorders.
Full disclosure, I'm a soccer fanatic.
"CCL11, a protein previously associated with age-associated cognitive decline, is observed to be increased in the brain and cerebrospinal fluid (CSF) in chronic traumatic encephalopathy (CTE) compared to Alzheimer’s disease (AD). Using a cohort of 23 deceased American football players with neuropathologically verified CTE, 50 subjects with neuropathologically diagnosed AD, and 18 non-athlete controls, CCL11 was measured with ELISA in the dorsolateral frontal cortex (DLFC) and CSF. CCL11 levels were significantly increased in the DLFC in subjects with CTE (fold change = 1.234, p < 0.050) compared to non-athlete controls and AD subjects with out a history of head trauma. This increase was also seen to correlate with years of exposure to American football (β = 0.426, p = 0.048) independent of age (β = -0.046, p = 0.824). Preliminary analyses of a subset of subjects with available post-mortem CSF showed a trend for increased CCL11 among individuals with CTE (p = 0.069) mirroring the increase in the DLFC. Furthermore, an association between CSF CCL11 levels and the number of years exposed to football (β = 0.685, p = 0.040) was observed independent of age (β = -0.103, p = 0.716). Finally, a receiver operating characteristic (ROC) curve analysis demonstrated CSF CCL11 accurately distinguished CTE subjects from non-athlete controls and AD subjects (AUC = 0.839, 95% CI 0.62–1.058, p = 0.028). Overall, the current findings provide preliminary evidence that CCL11 may be a novel target for future CTE biomarker studies."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5614644/
The next bit concerns Traumatic Brain Injury (TBI)...semantics, IMO. This has more mention of CCR5. Both are 5 years old or so.
"Traumatic brain injury (TBI) is defined as an open or closed head injury that disrupts brain function. Millions of people worldwide seek medical attention for TBI as a result of falls, motor vehicle accidents, sports- and war-related activities, among others. Depending on the etiology, TBIs can be closed head or penetrating, and occur in a single event or in a repetitive fashion [1]. Any of these types of injuries can result in various severities that are clinically classified as mild, moderate or severe based on a series of neurological tests [2]."
Abtract.
Traumatic brain injury (TBI) affects millions of people worldwide every year. The primary impact initiates the secretion of pro- and anti-inflammatory factors, subsequent recruitment of peripheral immune cells and activation of brain-resident microglia and astrocytes. Chemokines are major mediators of peripheral blood cell recruitment to damaged tissue, including the TBI brain. Here we review the involvement of specific chemokine pathways in TBI pathology and attempts to modulate these pathways for therapeutic purposes. We focus on chemokine (C-C motif) ligand 2/chemokine (C-C motif) receptor 2 (CCL2/CCR2) and chemokine (C-X-C motif) ligand 12/chemokine (C-X-C motif) receptor 4 (CXCL12/CXCR4). Recent micro-array and multiplex expression profiling have also implicated CXCL10 and CCL5 in TBI pathology. Chemokine (C-X3-C motif) ligand 1/ chemokine (C-X3-C motif) receptor 1 (CX3CL1/CX3CR1) signaling in the context of TBI is also discussed. Current literature suggests that modulating chemokine signaling, especially CCL2/CCR2, may be beneficial in TBI treatment."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4485943/
Total google search I think I put the smart parts in quotes.
Good Luck Y'all,
chazzle
I'm glad you mentioned CCL11. After some of the memory implications I was taking a look at over the weekend, I wanted to search CCR5 in CTE (chronic traumatic enchephalopathy) - largely as a follow up to a theory Ive been kicking around concerning inflammation in PTSD, concussions, depression, and others. Since Leronlimab down-regulates CCL11, perhaps we can have a positive effect for those suffering from CTE, or other brain affected inflammatory disorders.
Full disclosure, I'm a soccer fanatic.
"CCL11, a protein previously associated with age-associated cognitive decline, is observed to be increased in the brain and cerebrospinal fluid (CSF) in chronic traumatic encephalopathy (CTE) compared to Alzheimer’s disease (AD). Using a cohort of 23 deceased American football players with neuropathologically verified CTE, 50 subjects with neuropathologically diagnosed AD, and 18 non-athlete controls, CCL11 was measured with ELISA in the dorsolateral frontal cortex (DLFC) and CSF. CCL11 levels were significantly increased in the DLFC in subjects with CTE (fold change = 1.234, p < 0.050) compared to non-athlete controls and AD subjects with out a history of head trauma. This increase was also seen to correlate with years of exposure to American football (β = 0.426, p = 0.048) independent of age (β = -0.046, p = 0.824). Preliminary analyses of a subset of subjects with available post-mortem CSF showed a trend for increased CCL11 among individuals with CTE (p = 0.069) mirroring the increase in the DLFC. Furthermore, an association between CSF CCL11 levels and the number of years exposed to football (β = 0.685, p = 0.040) was observed independent of age (β = -0.103, p = 0.716). Finally, a receiver operating characteristic (ROC) curve analysis demonstrated CSF CCL11 accurately distinguished CTE subjects from non-athlete controls and AD subjects (AUC = 0.839, 95% CI 0.62–1.058, p = 0.028). Overall, the current findings provide preliminary evidence that CCL11 may be a novel target for future CTE biomarker studies."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5614644/
The next bit concerns Traumatic Brain Injury (TBI)...semantics, IMO. This has more mention of CCR5. Both are 5 years old or so.
"Traumatic brain injury (TBI) is defined as an open or closed head injury that disrupts brain function. Millions of people worldwide seek medical attention for TBI as a result of falls, motor vehicle accidents, sports- and war-related activities, among others. Depending on the etiology, TBIs can be closed head or penetrating, and occur in a single event or in a repetitive fashion [1]. Any of these types of injuries can result in various severities that are clinically classified as mild, moderate or severe based on a series of neurological tests [2]."
Abtract.
Traumatic brain injury (TBI) affects millions of people worldwide every year. The primary impact initiates the secretion of pro- and anti-inflammatory factors, subsequent recruitment of peripheral immune cells and activation of brain-resident microglia and astrocytes. Chemokines are major mediators of peripheral blood cell recruitment to damaged tissue, including the TBI brain. Here we review the involvement of specific chemokine pathways in TBI pathology and attempts to modulate these pathways for therapeutic purposes. We focus on chemokine (C-C motif) ligand 2/chemokine (C-C motif) receptor 2 (CCL2/CCR2) and chemokine (C-X-C motif) ligand 12/chemokine (C-X-C motif) receptor 4 (CXCL12/CXCR4). Recent micro-array and multiplex expression profiling have also implicated CXCL10 and CCL5 in TBI pathology. Chemokine (C-X3-C motif) ligand 1/ chemokine (C-X3-C motif) receptor 1 (CX3CL1/CX3CR1) signaling in the context of TBI is also discussed. Current literature suggests that modulating chemokine signaling, especially CCL2/CCR2, may be beneficial in TBI treatment."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4485943/
Total google search I think I put the smart parts in quotes.
Good Luck Y'all,
chazzle
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