scholarly journals Upregulation of Brain Renin Angiotensin System by 27-Hydroxycholesterol in Alzheimer's Disease

2011 ◽  
Vol 24 (4) ◽  
pp. 669-679 ◽  
Author(s):  
Laura Mateos ◽  
Muhammad-Al-Mustafa Ismail ◽  
Francisco-Javier Gil-Bea ◽  
Valerio Leoni ◽  
Bengt Winblad ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

scholarly journals Cerebrospinal Fluid Changes in the Renin-Angiotensin System in Alzheimer’s Disease

2019 ◽  
Vol 72 (2) ◽  
pp. 525-535 ◽  
Author(s):  
Patrick G. Kehoe ◽  
Noura Al Mulhim ◽  
Henrik Zetterberg ◽  
Kaj Blennow ◽  
James S. Miners
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

Research Progress of Alzheimer’s Disease Therapeutic Drugs: Based on Renin-Angiotensin System Axis

2020 ◽  
Vol 78 (4) ◽  
pp. 1315-1338
Author(s):  
Xinquan Li ◽  
Weiting Xuan ◽  
Dabao Chen ◽  
Huawu Gao ◽  
Guangyun Wang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Function ◽  
Amyloid Β ◽  
Renin Angiotensin System ◽  
Research Progress ◽  
Signal Peptides ◽  
Amyloid Β Protein ◽  
Angiotensin System ◽  
Renin Angiotensin

It is widely recognized that Alzheimer’s disease (AD) has a complicate link to renin-angiotensin system (RAS). It is known that cerebrovascular disease has some connections with AD, but most of the studies are still conducted in parallel or independently. Although previous research came up with large number of hypotheses about the pathogenesis of AD, it does not include the mechanism of RAS-related regulation of AD. It has been found that many components of RAS have been changed in AD. For example, the multifunctional and high-efficiency vasoconstrictor Ang II and Ang III with similar effects are changed under the action of other RAS signal peptides; these signal peptides are believed to help improve nerve injury and cognitive function. These changes may lead to neuropathological changes of AD, and progressive defects of cognitive function, which are association with some hypotheses of AD. The role of RAS in AD gradually attracts our attention, and RAS deserved to be considered carefully in the pathogenesis of AD. This review discusses the mechanisms of RAS participating in the three current hypotheses of AD: neuroinflammation, oxidative stress and amyloid-β protein (Aβ) hypothesis, as well as the drugs that regulate RAS systems already in clinical or in clinical trials. It further demonstrates the importance of RAS in the pathogenesis of AD, not only because of its multiple aspects of participation, which may be accidental, but also because of the availability of RAS drugs, which can be reused as therapies of AD.

The Renin Angiotensin System and Alzheimer's Disease

2000 ◽  
Vol 903 (1 VASCULAR FACT) ◽  
pp. 437-441 ◽  
Author(s):  
PHILIPPE AMOUYEL ◽  
FLORENCE RICHARD ◽  
CLAUDINE BERR ◽  
ISABELLE DAVID-FROMENTIN ◽  
NICOLE HELBECQUE
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

Renin-Angiotensin System Alterations in the Human Alzheimer’s Disease Brain

2021 ◽  
pp. 1-12
Author(s):  
Saifudeen Ismael ◽  
Golnoush Mirzahosseini ◽  
Heba A. Ahmed ◽  
Arum Yoo ◽  
Modar Kassan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Process ◽  
Renin Angiotensin System ◽  
Brain Diseases ◽  
Complex Nature ◽  
Postmortem Human Brain ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Protein Levels

Background: Understanding Alzheimer’s disease (AD) in terms of its various pathophysiological pathways is essential to unravel the complex nature of the disease process and identify potential therapeutic targets. The renin-angiotensin system (RAS) has been implicated in several brain diseases, including traumatic brain injury, ischemic stroke, and AD. Objective: This study was designed to evaluate the protein expression levels of RAS components in postmortem cortical and hippocampal brain samples obtained from AD versus non-AD individuals. Methods: We analyzed RAS components in the cortex and hippocampus of postmortem human brain samples by western blotting and immunohistochemical techniques in comparison with age-matched non-demented controls. Results: The expression of AT1R increased in the hippocampus, whereas AT2R expression remained almost unchanged in the cortical and hippocampal regions of AD compared to non-AD brains. The Mas receptor was downregulated in the hippocampus. We also detected slight reductions in ACE-1 protein levels in both the cortex and hippocampus of AD brains, with minor elevations in ACE-2 in the cortex. We did not find remarkable differences in the protein levels of angiotensinogen and Ang II in either the cortex or hippocampus of AD brains, whereas we observed a considerable increase in the expression of brain-derived neurotrophic factor in the hippocampus. Conclusion: The current findings support the significant contribution of RAS components in AD pathogenesis, further suggesting that strategies focusing on the AT1R and AT2R pathways may lead to novel therapies for the management of AD.

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