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.

Friday, July 10, 2026

Impact of inhalational anesthetics on neurodegeneration in Alzheimer’s disease: current evidence and potential implications

Will your competent? doctor at least ensure further research occurs that determines how and the interventions needed to make this work. You are an at-risk population or hasn't you doctor informed you of that?

Your risk of dementia, has your doctor told you of this?  Your doctor is responsible for preventing this! Is s/he willing to prevent this?

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here:

  Impact of inhalational anesthetics on neurodegeneration in Alzheimer’s disease: current evidence and potential implications

 Austin Dosanjh1,#, Sanarya Al-Jaf1,#, Emily Ye1,#, and Khaled S. Abd-Elrahman1,2,3,*  
1. Department of Anesthesiology, Pharmacology and Therapeutics, and Djavad  Mowafaghian Centre for Brain Health, The University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada  
2. Department of Medical Sciences, College of Medicine and Health Sciences, Khalifa  University, Abu Dhabi 127788, United Arab Emirates  
3. Department of Pharmacology and Toxicology, Faculty of Pharmacy, Alexandria  University, Alexandria 21521, Egypt  # Contributed equally to this work  * Address correspondence to:  Dr. Khaled S. Abd-Elrahman  Department of Anesthesiology, Pharmacology and Therapeutics  University of British Columbia  2176 Health Sciences Mall, Vancouver, British Columbia, V6T 1Z3.  Tel: 6048221390  khaled.abdelrahman@ubc.ca

Abstract 

Alzheimer’s disease is the most common form of dementia, primarily affecting the elderly population. It is a progressive neurodegenerative disease with key pathogenesis hallmarks being amyloid-beta plaque accumulation, and neurofibrillary tangles of tau protein. With an increasingly aging population and rising numbers of surgical procedures, growing interest has been directed towards the potential impact of inhalational anesthetics, particularly isoflurane, sevoflurane and desflurane, in contributing to the neurodegenerative process. Evidence supporting anesthetic-related modulation of  Alzheimer’s disease pathways is derived predominantly from in vitro and animal models, with comparatively limited and heterogeneous human biomarker and clinical data. This review will explore the various mechanisms by which these volatile anesthetics may contribute to the pathogenesis of neurodegeneration in the context of AD. This includes upregulation of beta-secretase 1 resulting in the formation of amyloid-beta oligomers and inhibition of tau dephosphorylation. While certain studies point towards a neuroprotective  effect of these anesthetics, the evidence remains inconsistent. Collectively, these findings support perioperative strategies focused on maintenance of normothermia, optimization of oxygenation, and judicious anesthetic exposure as practical measures to mitigate vulnerability in at-risk populations.

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