Lower circulating levels of angiotensin-converting enzyme (ACE) in patients with schizophrenia

Mohite, Satyajit; Campos-Carli, Salvina Maria de; Rocha, Natália Pessoa; Sharma, Shiva; Miranda, Aline Silva de; Barbosa, Izabela Guimarães; Salgado, João Vinícius; Simões‐e‐Silva, Ana Cristina; Teixeira, Antônio Lúcio

doi:10.1016/j.schres.2018.06.023

Cited by 24 publications

(13 citation statements)

References 37 publications

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“…Similar results were obtained with the administration of AT 1 receptor antagonists in patients and in experimental models of Alzheimer’s disease, Parkinson’s disease, stroke, traumatic brain injury, and spinal cord injury (Villapol and Saavedra, 2015). Our research group has investigated the profile of RAS molecules in the blood and/or cerebrospinal fluid (CSF) of patients with different neuropsychiatric conditions, including Parkinson’s disease (Rocha et al, 2016), Alzheimer’s disease (Rocha et al, 2018), and schizophrenia (Mohite et al, 2018). In patients with Parkinson’s disease, lower circulating levels of angiotensin II (Ang II) and Ang-(1–7) were associated with increased severity of depressive symptoms (Rocha et al, 2016).…”

Section: Brain-renal Axis: An Evolving Conceptmentioning

confidence: 99%

“…Patients with Alzheimer’s disease had decreased levels of ACE when compared with controls, and there was a significant positive correlation between ACE and amyloid-β 42 concentrations in the CSF of patients (Rocha et al, 2018). Patients with schizophrenia exhibited reduced circulating levels of ACE in comparison to controls (Mohite et al, 2018).…”

Section: Brain-renal Axis: An Evolving Conceptmentioning

confidence: 99%

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Neuropsychiatric Disorders in Chronic Kidney Disease

Silva

Miranda²,

Rocha

et al. 2019

Front. Pharmacol.

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Neuropsychiatric conditions including depression, anxiety disorders, and cognitive impairment are prevalent in patients with chronic kidney disease (CKD). These conditions often make worse the quality of life and also lead to longer hospitalizations and higher mortality. Over the past decades, some hypotheses have tried to explain the connection between CKD and neuropsychiatric disorders. The most common hypothesis is based on the occurrence of cerebrovascular disease and accumulated uremic toxins in adult patients with CKD. However, the lack of a direct association between known vascular risk factors (e.g., diabetes and hypertension) with CKD-related cognitive deficits suggests that other mechanisms may also play a role in the pathophysiology shared by renal and neuropsychiatric diseases. This hypothesis is corroborated by the occurrence of neuropsychiatric comorbidities in pediatric patients with CKD preceding vascular damage, and the inconsistent findings on neuroprotective effects of antihypertensives. The aim of this narrative review was to summarize clinical evidence and potential mechanisms that links CKD and brain disorders, specifically in regard to cognitive impairment, anxiety, and depression.

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Section: Brain-renal Axis: An Evolving Conceptmentioning

confidence: 99%

Section: Brain-renal Axis: An Evolving Conceptmentioning

confidence: 99%

Neuropsychiatric Disorders in Chronic Kidney Disease

Silva

Miranda²,

Rocha

et al. 2019

Front. Pharmacol.

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“…Over the past decades, accumulating evidence has pointed out the role for RAS components in neuropsychiatric disorders [for review see ( 49 , 51 , 65 , 66 )]. Our research group has extensively investigated the profile of RAS molecules in the blood and/or cerebrospinal fluid (CSF) of patients with different neurodegenerative and psychiatric conditions, including Parkinson's disease ( 67 ), Alzheimer's disease (AD) ( 68 ), and schizophrenia ( 69 ). For example, patients with Parkinson's disease presented decreased circulating levels of Ang II and Ang-(1-7) along with increased severity of depressive symptoms ( 67 ).…”

Section: Ace2-angiotensin (1-7)-mas Receptors Axis Role In Geriatric-mentioning

confidence: 99%

Coronavirus Disease-2019 Conundrum: RAS Blockade and Geriatric-Associated Neuropsychiatric Disorders

Miranda

Teixeira

2020

Front. Med.

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Coronavirus Disease 2019 (COVID-19) is caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which primarily targets the human respiratory system and may lead to severe pneumonia and ultimately death. Mortality rate is particurlarly high among people beyond the sixth decade of life with cardiovascular and metabolic diseases. The discovery that the SARS-CoV-2 uses the renin-angiotensin system (RAS) component ACE2 as a receptor to invade host epithelial cells and cause organs damage resulted in a debate regarding the role of ACE inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) therapies during COVID-19 pandemic. Some authors proposed the discontinuation of ACEIs and ARBs for cardiovascular, kidney, and metabolic diseases, while expert opinions have discouraged that due to limited empirical evidence of their negative effect on COVID-19 outcomes, and that withdrawing treatment may contribute to clinical decompensation in high-risk patients. Moreover, as cardiovascular and metabolic diseases are associated with neurodegenerative and psychiatric disorders, especially among older adults, a critical appraisal of the potential positive effects of ACEIs and ARBs is highly needed. Herein, we aim to discuss the conundrum of ACEIs and ARBs use in high-risk patients for COVID-19, and their potential protective role on the development and/or progression of geriatric neuropsychiatric disorders.

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“…For instance, PPARD has been shown to inhibit CB1 receptor expression (CNR1), which contributes to the pathophysiology of SCZ [17]. PPARD also reduces the upregulation of angiotensin II type 1 receptor (AGTR1) [18], the antagonists of which have been reported to improve clinical symptoms in SCZ patients [19]. In addition, PPARD activation promotes the degradation of aggrecan (ACAN) and attenuates gene expression of IL1B [20,21].…”

Section: Ppar Researchmentioning

confidence: 99%

PPARD May Play a Protective Role against the Development of Schizophrenia

Kapoor

et al. 2020

PPAR Research

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PPARD has been suggested to contribute to the etiology of schizophrenia (SCZ) with the underlying mechanisms largely unknown. Here, we first collected and analyzed the PPARD expression profile from three groups: (1) 18 healthy control (HC) subjects, (2) 14 clinical high-risk (CHR) patients, and (3) 19 early onset of SCZ (EOS) patients. After that, we conducted a systematical pathway analysis to explore the potential mechanisms involved in PPARD exerting influence on the pathological development of SCZ. Compared to the HC group, the expression of PPARD was slightly decreased in the EOS group (LFC=−0.34; p=0.23) and increased in the CHR group (LFC=0.65; p=0.20). However, there was a significant difference between the EOS group and the CHR group (LFC=−0.99; p=0.015), reflecting the amount of variation in PPARD expression before and after the onset of SCZ. Pathway analysis suggested that overexpression of PPARD may regulate ten proteins or molecules to inhibit the pathological development of SCZ, including the deactivation of eight SCZ promoters and stimulation of two SCZ inhibitors. Our results support the association between PPARD and SCZ. The pathways identified may help in the understanding of the potential mechanisms by which PPARD contributes to the etiology of SCZ.

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Lower circulating levels of angiotensin-converting enzyme (ACE) in patients with schizophrenia

Cited by 24 publications

References 37 publications

Neuropsychiatric Disorders in Chronic Kidney Disease

Neuropsychiatric Disorders in Chronic Kidney Disease

Coronavirus Disease-2019 Conundrum: RAS Blockade and Geriatric-Associated Neuropsychiatric Disorders

PPARD May Play a Protective Role against the Development of Schizophrenia

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