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.

Thursday, March 19, 2026

Renin-angiotensin system blockade attenuates brain mitochondrial dysfunction, oxidative stress, and neuroinflammation associated with hypertension, metabolic disorders, and aging

Your competent? doctor created protocols on this years ago, right? Oh NO! YOUR DOCTOR, HOSPITAL AND BOARD OF DIRECTORS ARE ALL COMPPLETELY INCOMPETENT!     

So, they actually prefer wallowing in their ignorance, doesn't require as much brainpower!

renin angiotensin system (2 posts to October 2016)

 Renin-angiotensin system blockade attenuates brain mitochondrial dysfunction, oxidative stress, and neuroinflammation associated with hypertension, metabolic disorders, and aging

 Sebastián García Menéndez, Felipe Inserra, Elena MV de Cavanagh, Leon Ferder, Walter Manucha Sebastián García Menéndez, Department of Pathology, Facultad de Ciencias Médicas, Universidad Nacional de Cuyo, Mendoza 5500, Argentina Felipe Inserra, Department of Postgraduate, Austral University, Pilar 1630, Argentina Elena MV de Cavanagh, Department of Postgraduate, Austral University Hospital, Arterial Hypertens Ctr, Sch Biomed Sci, CABA 1629, Argentina Leon Ferder, Department of Pharmacology, Universidad Maimónides, Ciudad Autónoma de Buenos Aires C1405, Argentina Walter Manucha, Department of Pathology, Institute of Medicine and Experimental Biology of Cuyo, National Council for Scientific and Technological Research, National University of Cuyo, Laboratory of Basic and Translational Experimental Pharmacology, Faculty of Medical Sciences, Mendoza 5500, Argentina ORCID number: Walter Manucha (0000-0002-2279-7626). Author contributions: García Menéndez S, Inserra F, de Cavanagh EMV, Ferder L and Manucha W were responsible for writing, discussion and preparation of this manuscript, and have also read and approved the final version of the manuscript. Conflict-of-interest statement: The authors declare that they have no conflict of interest. Corresponding author: Walter Manucha, PhD, Professor, Department of Pathology, Institute of Medicine and Experimental Biology of Cuyo, National Council for Scientific and Technological Research, National University of Cuyo, Laboratory of Basic and Translational Experimental Pharmacology, Faculty of Medical Sciences, Avenue El Libertador 80, Mendoza 5500, Argentina. wmanucha@yahoo.com.ar Received: August 20, 2025 Revised: October 25, 2025 Accepted: January 20, 2026 Published online: March 20, 2026 Processing time: 207 Days and 13.6 Hours 

 Abstract 


Although aging is an inherent part of life, it represents a process of progressive dysfunction rather than a fixed biological outcome. Consequently, highly prevalent conditions such as cardiorenal-metabolic syndrome-which encompasses obesity, hypertension (HTN), and metabolic disorders-can accelerate age-related changes. The renin-angiotensin system (RAS) plays a critical role in pathophysiology and affects multiple organs, including the brain. The central nervous system contains both RAS branches: The ACE/Ang II/AT1 and AT2 receptor axis, as well as the ACE2/Ang-(1-7)/Mas receptor axis. Neuroinflammation is a chronic process characterized by glial cell activation triggered by increased production of reactive oxygen and nitrogen species, resulting in oxidative stress. Mitochondria are the primary cellular sites where these processes occur. Under conditions such as metabolic disorders, obesity, HTN, and aging, these reactions are markedly accelerated. Associated mechanisms include insulin resistance, elevated levels of advanced glycation end-products, and disruption of the blood-brain barrier. The consequences of these alterations may include brain dysfunction, cognitive decline, Parkinson’s disease, and neurodegenerative conditions such as Alzheimer’s disease. This review focuses on the primary effects of therapeutic interventions on mitochondrial function, with particular attention to the modulation of oxidative stress, chronic neuroinflammation, and glial dysregulation. We highlight the strategic use of angiotensin receptor blockers and ACE2 activators as promising tools that may redefine the prevention and treatment of vascular dementia and other neurodegenerative diseases of inflammatory origin. 

 Key Words: Renin-angiotensin system blockade; Oxidative stress; Central nervous system inflammation; Neurodegeneration; Hypertension; Metabolic disorders; Mitochondria; Aging Core Tip: This study highlights renin-angiotensin system blockade as a promising strategy for preventing brain damage associated with hypertension, metabolic disorders, and aging. These conditions accelerate mitochondrial dysfunction, oxidative stress, and neuroinflammation. Our work focuses on the strategic use of angiotensin receptor blockers and ACE2 activators, demonstrating their potential to mitigate these pathological processes and offering a novel avenue for the prevention and treatment of vascular dementia and other neurodegenerative diseases. Citation: García Menéndez S, Inserra F, de Cavanagh EM, Ferder L, Manucha W. Renin-angiotensin system blockade attenuates brain mitochondrial dysfunction, oxidative stress, and neuroinflammation associated with hypertension, metabolic disorders, and aging. World J Exp Med 2026; 16(1): 113259 URL: https://www.wjgnet.com/2220-315x/full/v16/i1/113259.htm DOI: https://dx.doi.org/10.5493/wjem.v16.i1.113259

García Menéndez S, Inserra F, de Cavanagh EM, Ferder L, Manucha W. Renin-angiotensin system blockade attenuates brain mitochondrial dysfunction, oxidative stress, and neuroinflammation associated with hypertension, metabolic disorders, and aging. World J Exp Med 2026; 16(1): 113259 [DOI: 10.5493/wjem.v16.i1.113259]

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