Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 32,712 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.
Tuesday, April 7, 2026
Copper depletion ameliorates neuronal damage after intracerebral hemorrhage
Will your competent? doctor DO ANYTHING AT ALL WITH THIS?
NO? So, doesn't care about your recovery at all! Won't get human testing going either?
Do you
prefer your doctor, hospital and board of director's incompetence NOT
KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand
action!
OH NO! your doctor KNOWS NOTHING AND DOES NOTHING!
Intracerebral hemorrhage (ICH) induces copper overload and cuproptosis in perihematomal brain tissue.
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The copper chelator TTM mitigates copper accumulation and inhibits cuproptosis in vivo and in vitro.
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Copper depletion with TTM alleviates ICH-induced brain injury and neuronal death.
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TTM treatment promotes the expression of neurite regeneration-associated proteins GAP43 and MAP2.
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Targeting copper-induced cuproptosis is a promising therapeutic strategy for ICH.
Abstract
Background
Intracerebral hemorrhage (ICH) is a severe subtype of stroke. There are currently no specific treatment strategies for secondary brain injury and neurological deficits following ICH. Copper (Cu) is an essential cofactor for all living organisms. Cytotoxicity can occur when copper ion concentration exceeds the homeostatic threshold, leading to cell death. However, the relationship between copper and ICH is unclear.
Methods
In vivo, an ICH model was established in male Sprague-Dawley rats by stereotactically injecting autologous blood into the right basal ganglia. In vitro, we employed hemin and CuCl2 to simulate ICH conditions and induce cuproptosis in BV2 microglial cells. To investigate the role of copper in brain injury and neuronal damage, we administered the copper chelator tetrathiomolybdate (TTM) and knocked down the essential cuproptosis gene ferredoxin 1 (FDX1).
Results
Our findings demonstrate that following ICH, elevated copper levels and FDX1 expression, low expression of lipoylated dihydrolipoamide S-acetyltransferase (DLAT) and lipoic acid synthetase (LIAS), loss of mitochondrial membrane potential and neuronal impairment (increased growth associated protein 43 (GAP43) and decreased microtubule associated protein 2 (MAP2) expression), ultimately lead to neuronal death. Both TTM and si-FDX1 treatment attenuated the copper overload and inhibited cuproptosis, thereby ameliorating the ICH-induced phenotype.
Conclusion
Copper depletion attenuates ICH-induced neuronal damage by inhibiting cuproptosis, highlighting a potential therapeutic strategy for mitigating secondary brain injury and neuronal damage following ICH.
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