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, February 27, 2026

Neuroprotective Effect of Combined Pomegranate and Candesartan Therapy Against Chronic Cerebral Ischemia in Rats

Your competent? doctor already has a pomegranate protocol, right? And a Candarsartan  protocol, right? I don't care that this is in rats, doesn't your doctor want to recover stroke survivors regardless of where the research was accomplished? Oh, but I guess your doctor doesn't read research, SO INCOMPETENT THEN!
Oh, nothing was done; SO FUCKING INCOMPETENCE THEN?

 Neuroprotective Effect of Combined Pomegranate and Candesartan Therapy Against Chronic Cerebral Ischemia in Rats

Rana Awada1,2, Fatima Radi1, Zaher Abdel Baki3, Akram Hijazi1, Wissam H. Joumaa2, Zeinab Ezzeddine6, Laurent. O. Martinez4,5*, Mohamad Nasser1,2,4,5* 1 Doctoral School of Science and Technology, Research Platform for Environmental Science (PRASE), Lebanese university, Lebanon; 2Anti-Cancer Therapeutic Approaches Group (ATAC), Rammal Hassan Rammal Research Laboratory Biology Department, Faculty of Sciences, Lebanese University, Lebanon 3 College of Engineering and Technology, American University of the Middle East, Egaila 54200, Kuwait 4 LiMitAging team, Institute of Metabolic and Cardiovascular Diseases, I2MC, Université de Toulouse, INSERM, UMR1297, 31000 Toulouse, France 5IHU HealthAge, 31000 Toulouse, France 6 High Council for Scientific Research & Publication (HCSRP), Islamic University of Lebanon (IUL), Khalde P.O. Box 30014, Lebanon *Corresponding Authors: mohamad.nasser@inserm.fr (Mohamad Nasser) Laurent.martinez@inserm.fr (Laurent Martinez) 
 Keywords: Aging, Stroke, Chronic Cerebral ischemia, Candesartan, Pomegranate, Neuroprotection, Sensorimotor function Abstract The copyright holder for this bioRxiv preprint doi: https://doi.org/10.64898/2026.02.23.707366 ; this version posted February 24, 2026. preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 
 Background: 
Stroke remains a leading cause of mortality worldwide. Ischemic stroke, caused by arterial occlusion, induces sensorimotor deficits and memory impairments. Excessive activity of the brain angiotensin II type 1 receptor (AT1R) is associated with hypertension and cerebral ischemia. Candesartan (CN), an AT1R blocker, improves cerebrovascular blood flow. Pomegranate (Punica granatum) is rich in polyphenolic antioxidants that reduce oxidative stress and inflammation, suggesting potential neuroprotective effects in cerebral ischemia. Aim: This study compared the neuroprotective effects of CN administered alone or in combination with pomegranate (POM) in a rat model of cerebral ischemia induced by chronic unilateral carotid artery ligation. 

Methods: 
Cerebral ischemia was induced by ligation of the right common carotid artery (RCCA) in adult rats. Animals were randomly assigned to four groups: sham control, untreated ischemic, ischemic treated with CN, and ischemic treated with CN + POM. Sensorimotor and cognitive functions were assessed 1–15 days post-surgery using beam balance (BB), beam walking (BW), modified sticky-tape (MST), novel object recognition (NOR), and the Morris water maze (MWM) tests. 

Results: 
RCCA ligation induced marked sensorimotor deficits and memory impairments. Both CN monotherapy and CN + POM treatment equally restored sensorimotor function to sham-control levels, as demonstrated by BB, BW, and MST tests. In contrast, CN + POM treatment showed greater efficacy than CN alone in improving short-term recognition and spatial memory, as demonstrated by NOR and MWM performance. 
Conclusion: 
CN effectively reverses ischemia-induced sensorimotor deficits, whereas the addition of POM confers specific and enhanced protection against cognitive impairment, indicating distinct mechanisms underlying sensorimotor and memory recovery after cerebral ischemia.

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