Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 31,822 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
Wednesday, December 3, 2025
Nanomedicine in neurotrauma: A comprehensive review of gold nanoparticles for traumatic brain injury treatment
I bet your fuckingly incompetent? doctor hasn't implemented gold nanoparticles in the past 4 years? And your board of directors is so incompetent they don't even know how to run a stroke hospital!
Send me personal hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name(If you can't stand by your name don't bother replying anonymously) and my response in my blog. Or are you afraid to engage with my stroke-addled mind? No excuses are allowed! You're medically trained; it should be simple to precisely state EXACTLY WHY you aren't working on 100% recovery protocols with NO EXCUSES!
TBI treatment using gold nanoparticles (AuNPs) is multi-mechanistic.
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AuNPs have intrinsic anti-inflammatory and antioxidant properties across the blood-brain barrier.
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They stimulate neuroregeneration via PI3K/Akt and MAPK/ERK.
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Drug, growth factor, and genetic material can be targeted via functionalized AuNPs.
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Preclinical studies demonstrate less lesions, less inflammation, and better cognition.
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Standardization, toxicity, and manufacturing must be addressed in clinical translation.
Abstract
Traumatic brain injury (TBI) remains an enormous source of mortality and morbidity worldwide with few therapeutic options available today that address the pathophysiology of neuroinflammation, oxidative stress, and disruption of the blood-brain barrier (BBB) effectively. One of the promising classes of nanomedicines being explored extensively today for the treatment of TBI is gold nanoparticles (AuNPs) due to their biocompatibility, ability to target the BBB effectively, and versatility with respect to modification of their surface chemistry. This tutorial review will examine the multifunctional aspects of AuNPs that make them an attractive therapeutic target in the treatment of TBI, with special attention being given to their application in the management of secondary brain injury. AuNPs possess potent anti-inflammatory properties that result from modulating the polarization of microglia toward the restorative M2 subtype combined with the inhibition of the NF-κB signaling pathway. Additionally, AuNPs possess the capacity to counter the disruptive effects of ROS on cells by scavenging them while boosting the levels of the endogenously produced antioxidants. Finally, AuNPs possess the capacity to contribute toward the repair of the neuronal cells of the brain by inducing the growth of neurites with the activation of the PI3K/Akt signaling axis while functioning as vectors of neurotrophins such as NGF/BDNF and siRNA. Preclinical trials utilizing AuNPs illustrate their capacity to inhibit the growth of the lesion area, the activation of glia cells, and the reduction of cognitive impairment combined with the preservation of the integrity of the BBB with enhanced levels of angiogenesis. Despite these breakthroughs made toward the development of AuNP therapeutic agents that target TBI pathologically, there remain issues that must be considered if these therapeutic agents are to emerge safely.
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