Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective 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.

Sunday, March 23, 2025

The chemotherapy agent doxorubicin induces CNS expression of Ascl1, a regulator of adult neurogenesis and differentiation

 Do you really think your stroke medical 'professionals' have seen this and initiated research into human stroke subjects? I don't!

Do you prefer your doctor and hospital incompetence being NOT KNOWING. Or NOT DOING?

The chemotherapy agent doxorubicin induces CNS expression of Ascl1, a regulator of adult neurogenesis and differentiation

Abstract

Cancer-related cognitive impairment (CRCI) is a common side effect of cancer and its treatments. Cancer chemotherapy has been associated with hippocampal dysfunction and memory impairment. We investigated the effects of one chemotherapy agent, doxorubicin, on the transcription factor Ascl1 and proliferation of stem cells in the brain. We used an inducible mouse model designed to express TdTomato in Ascl1-lineage cells. Five to six-month-old Ascl1-CreERT2:ROSA mice were treated peripherally with a single dose of either doxorubicin (10 mg/kg) or DMSO control (n = 9 per group, n = 4–5 per sex). We analyzed brains of mice that had been exposed to doxorubicin for 2 weeks and had induced Ascl1 expression after the first week. We used immunostaining of neurogenesis stage specific markers to evaluate the doxorubicin effects on neuronal differentiation in the dentate gyrus of the hippocampus. Overall, doxorubicin significantly increased Ascl1 expression by 81% at this time point. As measured by Ascl1 double stains with Sox2, GFAP, and NeuroD1, doxorubicin-treated mice experienced an increase in Ascl1-mediated neural proliferation compared to control. A similar significant increase in the number of Ascl1-expressing cells (by 146%) after doxorubicin treatment was observed in the gray matter of the cerebral cortex. Thus, rather than leading to the loss of developing neurons, we found that a single dose of doxorubicin increased their appearance and progression, suggesting that hippocampal losses from chemotherapies may require greater and more sustained damage.



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