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

Table 1 A summary of preclinical and clinical studies on renin-angiotensin system inhibition and neuroinflammation

Ref.	Model	Active intervention	Effects
Dong et al[109]	Epilepsia	Captopril	Attenuation of glial activation and inhibition of complement C3-C3a receptor
Affram et al[110]	Microglial activation by lipopolysaccharides	Telmisartan	Attenuation of glial activation
Quan et al[111]	Microglia-induced neurotoxic A1 astrocyte conversion associated with Alzheimer’s and Parkinson’s disease	Telmisartan	Reduction of NF-κB/p65 phosphorylation and expression via a PPARγ-dependent mechanism
Liu et al[112]	Mouse models of Parkinson's disease	ACE2 knockout mice and cell cultures	Activating the ACE2/MasR pathway reduces inflammation in microglial cells
Martín Giménez et al[39]	Nanopharmacology and RAS modulation	Nanoparticulate delivery systems designed for crossing the BBB	Enhance the bioavailability, selectivity, and effectiveness of compounds
Hajjar et al[113]	Older patients with mild cognitive impairment, characterized by executive dysfunction	Comparison of candesartan and lisinopril	Improvements in executive function and memory in the candesartan group after 12 months of treatment
Lee et al[114]	The incidence of AD in patients with coronary disease	Comparison of RAS inhibition users and non-users	ARBs significantly reduced the risk of AD, while ACEIs were not significantly associated with the risk of AD

ACEIs: Angiotensin-converting-enzyme inhibitors; ARBs: Angiotensin receptor blockers; AD: Alzheimer’s disease; BBB: Blood-brain barrier; RAS: Renin-angiotensin system.