Anxiety in obesity: Is neuroinflammation the critical link?

Sanchez, Kevin; Guerin, Steven

doi:10.1016/j.bbi.2019.01.008

Cited by 3 publications

(2 citation statements)

References 9 publications

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“…A diminished expression of ADIPOQ in our subjects with dementia, coupled with MMSE scores indicative of severe cognitive decline, further reinforces the gene's putative role in neurodegeneration. The relative fold change, determined by real-time PCR, showed a decrease in the dementia group, mirroring the findings of other studies reporting reduced ADIPOQ activity in Alzheimer's disease subjects compared to non-AD individuals (21,22).…”

Section: Discussionsupporting

confidence: 86%

Pathophysiology Crossroads: Examining the Role of Adiponectin (ADIPOQ) in the Intersection of Type II Diabetes and Dementia

Shakir,

Sana,

Aziz

et al. 2024

JHRR

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Background: Type II Diabetes Mellitus (Type II DM) is intricately linked with an increased risk of cognitive impairment and dementia. The ADIPOQ gene encodes adiponectin, a hormone that plays a critical role in glucose regulation and fatty acid oxidation and may be implicated in the pathophysiology of both diabetes and dementia. Understanding the expression of ADIPOQ in diabetic patients with dementia could offer insights into the mechanisms at play and aid in the development of potential therapeutic targets. Objective: This study aims to analyze the expression of the ADIPOQ gene in diabetic patients diagnosed with dementia and to correlate these findings with cognitive impairment as assessed by Mini-Mental State Examination (MMSE) scores. Methods: We collected 5ml EDTA blood samples from 88 diabetic dementia patients and 12 healthy controls after obtaining written informed consent. The study adhered to the Declaration of Helsinki guidelines. Serum adiponectin levels were measured via Chemiluminescent immunoassay (CLIA), and genomic DNA was isolated for methylation-specific PCR and expression analysis. ADIPOQ gene expression was quantified using real-time PCR, and data were analyzed using SPSS version 25, employing descriptive and inferential statistics. Results: The diabetic dementia patient group demonstrated significantly lower adiponectin levels (5.62 ± 1.08 µg/mL) and MMSE scores (10.68 ± 4.56) compared to healthy controls (adiponectin: 15.68 ± 4.64 µg/mL, MMSE: 25.9 ± 3.12). Real-time PCR results indicated a relative fold decrease of 4.9 in ADIPOQ gene expression in the dementia cohort. Conclusion: The ADIPOQ gene expression is inversely associated with cognitive function in diabetic patients, highlighting its potential as a biomarker for early detection and targeted therapeutic interventions in dementia associated with diabetes.

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Section: Discussionsupporting

confidence: 86%

Pathophysiology Crossroads: Examining the Role of Adiponectin (ADIPOQ) in the Intersection of Type II Diabetes and Dementia

Shakir,

Sana,

Aziz

et al. 2024

JHRR

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“…Neuroinflammation, PPARs, and Anxiety. Recently, the theory of neuroinflammation as the cause of anxiety development was discussed [138][139][140][141]. We performed a signal pathway analysis which revealed possible mechanism explaining the role of PPARs in the development of neuroinflammation (Figure 4).…”

Section: Enrichment Analysismentioning

confidence: 99%

Role of PPARs in Progression of Anxiety: Literature Analysis and Signaling Pathways Reconstruction

et al. 2020

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Peroxisome proliferator-activated receptor (PPAR) group includes three isoforms encoded by PPARG, PPARA, and PPARD genes. High concentrations of PPARs are found in parts of the brain linked to anxiety development, including hippocampus and amygdala. Among three PPAR isoforms, PPARG demonstrates the highest expression in CNS, where it can be found in neurons, astrocytes, and glial cells. Herein, the highest PPARG expression occurs in amygdala. However, little is known considering possible connections between PPARs and anxiety behavior. We reviewed possible connections between PPARs and anxiety. We used the Pathway Studio software (Elsevier). Signal pathways were created according to previously developed algorithms. SNEA was performed in Pathway Studio. Current study revealed 14 PPAR-regulated proteins linked to anxiety. Possible mechanism of PPAR involvement in neuroinflammation protection is proposed. Signal pathway reconstruction and reviewing aimed to reveal possible connection between PPARG and CCK-ergic system was conducted. Said analysis revealed that PPARG-dependent regulation of MME and ACE peptidase expression may affect levels of nonhydrolysed, i.e., active CCK-4. Impairments in PPARG regulation and following MME and ACE peptidase expression impairments in amygdala may be the possible mechanism leading to pathological anxiety development, with brain CCK-4 accumulation being a key link. Literature data analysis and signal pathway reconstruction and reviewing revealed two possible mechanisms of peroxisome proliferator-activated receptors involvement in pathological anxiety: (1) cytokine expression and neuroinflammation mechanism and (2) regulation of peptidases targeted to anxiety-associated neuropeptides, primarily CCK-4, mechanism.

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Cannabidiol ameliorates the anxiogenic and compulsive-like behaviors induced by chronic consumption of a high-carbohydrate diet in male mice

et al. 2022

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Anxiety in obesity: Is neuroinflammation the critical link?

Cited by 3 publications

References 9 publications

Pathophysiology Crossroads: Examining the Role of Adiponectin (ADIPOQ) in the Intersection of Type II Diabetes and Dementia

Pathophysiology Crossroads: Examining the Role of Adiponectin (ADIPOQ) in the Intersection of Type II Diabetes and Dementia

Role of PPARs in Progression of Anxiety: Literature Analysis and Signaling Pathways Reconstruction

Cannabidiol ameliorates the anxiogenic and compulsive-like behaviors induced by chronic consumption of a high-carbohydrate diet in male mice

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