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.

Monday, October 5, 2026

COLCHICINE INDUCED NEURODEGENERATION

Have your competent? doctor review this because of all the previous results of benefits! 

And come back with EXACT PROTOCOLS!

colchicine (28 posts to December 2011)

 COLCHICINE INDUCED NEURODEGENERATION

Poornima Yadav 1 , Priyanka Gupta Tahniyat Ansari 1 1 , Rupal Shukla & Sudhi Shrivastava 2 1 , 1Research Scholar & 2Assistant Professor Department of Zoology, CMP College, University of Allahabad, Prayagraj, Uttar Pradesh, India E-mail: sudhitp20@gmail.com 

 Abstract 


 Colchicine is an anti-inflammatory drug. It is a naturally occurring alkaloid derived from the Autumn Crocus plant, and has a long history of therapeutic use in treating gout, familial Mediterranean fever, and pericarditis. Its primary mechanism of action involves disrupting tubulin, which in turn modulates multiple inflammatory pathways. This disruption reduces neutrophil activity and migration across the vascular endothelium. The colchicine-induced neurodegeneration model is used to study Alzheimer’s disease (AD) because it mimics its key symptoms, including memory loss and damage to cholinergic neurons. This type of model helps in understanding the disease and in developing potential treatments. In AD patients, neurodegeneration is not limited to one area of the brain. Other brain areas, such as the corpus striatum and parietal cortex, exhibit amyloid plaques, and the amygdala undergoes atrophy, as observed in the MRI studies. This review aims to provide a comprehensive overview of the current state of knowledge on colchicine induced neurodegeneration in the brain. We discuss the mechanisms underlying colchicine's neurotoxic effects, including its disruption of microtubule dynamics, inhibition of the NLRP3 inflammasome (part of the innate immune system), and induction of oxidative stress. We also explore the evidence for colchicine-induced neurodegeneration in various animal models, including rats and fishes, and discuss the implications for human health. 

 Keywords: Colchicine, Neurotoxic, Neurodegeneration, Alzheimer’s Disease, Cognitive Decline Graphical Abstract Volume- 4, Issue- 1, January-June, 2026

Diagram at the link.
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