Metabolic Syndrome and Cognitive Function

Tahmi, Mouna; Palta, Priya; Luchsinger, José A.

doi:10.1007/s11886-021-01615-y

Cited by 32 publications

(27 citation statements)

References 75 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Our work has some strengths, to our knowledge it was one of the first studies that compares genetic polymorphisms, comorbidities, HIV-related values, and neurocognitive outcomes in HIV-infected patients. Previously, several authors studied the possible correlation between genetic polymorphisms, comorbidities or HIV-related values and neurocognitive outcomes in PWH (Foley et al 2010 ; Fogel et al 2015 ; Monroe et al, 2017; Callisaya et al 2019 ; Sun et al 2020 ; Buyo et al 2020 ; Levine et al, 2020 ; Ojeda-Juarez and Kaul, 2021 ; Xu et al 2021 ; Tahmi et al 2021 ). Notwithstanding, the combination of cognitive and physical functionality with genetic, comorbidities and HIV related values has never been assessed.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, HAND may be driven by several mechanisms, HIV-induced inflammation probably being the main driving factor, while ART, comorbidities, life-style and genetic background being possible exacerbating determinants. While genetic susceptibility is a non-modifiable risk factor for cognitive impairment, modifiable risk factors provide an opportunity for intervention and prevention of cognitive ability alterations and they have been studied in both HIV-infected and uninfected individuals (Foley et al 2010 ; Fogel et al 2015 ; Callisaya et al 2019 ; Sun et al 2020 ; Buyo et al 2020 ; Xu et al 2021 ; Tahmi et al 2021 ).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

An exploratory pilot study on the involvement of APOE, HFE, C9ORF72 variants and comorbidities in neurocognitive and physical performance in a group of HIV-infected people

et al. 2022

View full text Add to dashboard Cite

Cognitive decline of aging is modulated by chronic inflammation and comorbidities. In people with HIV-infection (PWH) it may also be affected by HIV-induced inflammation, lifestyle and long-term effects of antiretroviral therapies (ART). The role of genetics in the susceptibility to HIV-associated neurocognitive disorders (HAND) is not fully understood. Here we explored the possible relations among variants in 3 genes involved in inflammation and neurodegenerative disorders (APOE: ε2/ε3/ε4; HFE: H63D; C9ORF72: hexanucleotide expansions ≥ 9 repeats), cognitive/functional impairment (MiniMental State Examination MMSE, Clock Drawing Test CDT, Short Physical Performance Battery SPPB), comorbidities and HIV-related variables in a cohort of > 50 years old PWH (n = 60) with at least 10 years efficient ART. Patients with diabetes or hypertension showed significantly lower MMSE (p = .031) or SPPB (p = .010) scores, respectively, while no relations between HIV-related variables and cognitive/functional scores were observed. Patients with at least one APOEε3 allele had higher CDT scores (p = .019), APOEε2/ε4 patients showing the lowest scores in all tests. Patients with HFE-H63D variant showed more frequently hypertriglyceridemia (p = .023) and those harboring C9ORF72 expansions > 9 repeats had higher CD4+-cell counts (p = .032) and CD4% (p = .041). Multiple linear regression analysis computed to verify possible associations among cognitive/functional scores and all variables further suggested positive association between higher CDT scores and the presence of at least one APOEε3 allele (2,2; 95% CI [0,03 0,8]; p = .037), independent of other variables, although the model did not reach the statistical significance (p = .14). These data suggest that in PWH on efficient ART cognitive abilities and physical performances may be partly associated with comorbidities and genetic background. However, further analyses are needed to establish whether they could be also dependent and influenced by comorbidities and genetic background.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

An exploratory pilot study on the involvement of APOE, HFE, C9ORF72 variants and comorbidities in neurocognitive and physical performance in a group of HIV-infected people

et al. 2022

View full text Add to dashboard Cite

show abstract

“…Metabolic syndrome was associated with a higher risk for cognitive impairment that was observed across several studies. More particularly, higher triglyceride levels, higher systolic blood pressure, and a greater waist circumference were the strongest predictors of cognitive function in persons with schizophrenia [303], comparable with those of persons with metabolic syndrome [304]. The role of oxytocin in cognitive impairment through its regulation on the hippocampus, amygdala, and prefrontal cortex has been demonstrated in studies on oxytocin-knockout mice and studies on oxytocin receptor polymorphism in humans.…”

Section: Oxytocin Dysfunction As a Common Mechanism Underlying Schizo...mentioning

confidence: 93%

Crosstalk between Schizophrenia and Metabolic Syndrome: The Role of Oxytocinergic Dysfunction

Goh

Chen

et al. 2022

IJMS

View full text Add to dashboard Cite

The high prevalence of metabolic syndrome in persons with schizophrenia has spurred investigational efforts to study the mechanism beneath its pathophysiology. Early psychosis dysfunction is present across multiple organ systems. On this account, schizophrenia may be a multisystem disorder in which one organ system is predominantly affected and where other organ systems are also concurrently involved. Growing evidence of the overlapping neurobiological profiles of metabolic risk factors and psychiatric symptoms, such as an association with cognitive dysfunction, altered autonomic nervous system regulation, desynchrony in the resting-state default mode network, and shared genetic liability, suggest that metabolic syndrome and schizophrenia are connected via common pathways that are central to schizophrenia pathogenesis, which may be underpinned by oxytocin system dysfunction. Oxytocin, a hormone that involves in the mechanisms of food intake and metabolic homeostasis, may partly explain this piece of the puzzle in the mechanism underlying this association. Given its prosocial and anorexigenic properties, oxytocin has been administered intranasally to investigate its therapeutic potential in schizophrenia and obesity. Although the pathophysiology and mechanisms of oxytocinergic dysfunction in metabolic syndrome and schizophrenia are both complex and it is still too early to draw a conclusion upon, oxytocinergic dysfunction may yield a new mechanistic insight into schizophrenia pathogenesis and treatment.

show abstract

“…After biochemical remission, many symptoms and quality of life (QoL) improve, but significant morbidity and decreased QoL persist compared to healthy controls and patients treated for other pituitary adenomas 2 . In addition to the cardiovascular and metabolic morbidity of hypercortisolism, patients experience psychological and cognitive impairments 3 . The cause of psychological morbidity in CS patients is likely multifaceted, and the effects of glucocorticoid excess, chronic disease per se, and cardiovascular comorbidities are likely involved 2,3 .…”

Section: Endogenous Hypercortisolism and Exogenously Induced Glucocor...mentioning

confidence: 99%

“…2 In addition to the cardiovascular and metabolic morbidity of hypercortisolism, patients experience psychological and cognitive impairments. 3 The cause of psychological morbidity in CS patients is likely multifaceted, and the effects of glucocorticoid excess, chronic disease per se, and cardiovascular comorbidities are likely involved. 2,3 Conversely, altered hypothalamic-pituitary-adrenal (HPA) axis functioning has also been related to different psychiatric disease and cognitive impairment.…”

Section: Endogenous Hypercortisolism and Exogenously Induced Glucocor...mentioning

confidence: 99%

Long‐term effects of glucocorticoid excess on the brain

Dekkers

Amaya

Meulen

et al. 2022

J Neuroendocrinology

View full text Add to dashboard Cite

The metabolic and cardiovascular clinical manifestations in patients with Cushing's syndrome (CS) are generally well known. However, recent studies have broadened the perspective of the effects of hypercortisolism, showing that both endogenous and exogenous glucocorticoid excess alter brain functioning on several time scales. Consequently, cognitive deficits and neuropsychological symptoms are highly prevalent during both active CS and CS in remission, as well as during glucocorticoid treatment. In this review, we discuss the effects of endogenous hypercortisolism and exogenously induced glucocorticoid excess on the brain, as well as the prevalence of cognitive and neuropsychological deficits and their course after biochemical remission. Furthermore, we propose possible mechanisms that may underly neuronal changes, based on experimental models and in vitro studies. Finally, we offer recommendations for future studies.

show abstract

Metabolic Syndrome and Cognitive Function

Cited by 32 publications

References 75 publications

An exploratory pilot study on the involvement of APOE, HFE, C9ORF72 variants and comorbidities in neurocognitive and physical performance in a group of HIV-infected people

An exploratory pilot study on the involvement of APOE, HFE, C9ORF72 variants and comorbidities in neurocognitive and physical performance in a group of HIV-infected people

Crosstalk between Schizophrenia and Metabolic Syndrome: The Role of Oxytocinergic Dysfunction

Long‐term effects of glucocorticoid excess on the brain

Contact Info

Product

Resources

About