Executive function deficit in betel-quid-dependent chewers: Mediating role of prefrontal cortical thickness

Zhu, Xueling; Liu, Shaohui; Liao, Weihua; Kong, Lingyu; Jiang, Canhua; Fang, Yuan

doi:10.1177/0269881118806299

Cited by 12 publications

(24 citation statements)

References 90 publications

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“…NoGo-Go trials (NC>BQD) None online games (59,60). In the field of BQ addiction, our group study investigated the relationship between cortical thickness and executive function in chronic chewers with BQD, suggesting that BQD group had thinner cortex in bilateral PFC, and cortical thickness of the bilateral dorsolateral PFC mediated the correlation of betel-quid chewing and executive function (19). Consistent with decreased gray matter volumes in bilateral dorsolateral PFC and ventral medial PFC (22), results suggested that structural alteration in PFC in BQ users with BQD.…”

Section: Discussionmentioning

confidence: 99%

“…Second, animal studies suggested that high dose of BQ use could induce cocaine-like physiological states, such as anxiety, dilated pupils, tachycardia, and elevated blood pressure (16). In addition, BQ use was reported to be associated with altered cognitive ability, including spatial short-term memory (17), attention and inhibition control (18), executive function (19) and attention bias to BQ cues (20).…”

Section: Introductionmentioning

confidence: 99%

“…Recently, a review systematically assessed previous functional magnetic resonance imaging (fMRI) studies on BQ addiction, and suggested that a key involvement of the prefrontal cortex (PFC) in BQ dependency (21). For example, studies from our group suggested that BQ use was associated with decreased gray matter volumes in bilateral dorsolateral PFC and ventral medial PFC (22), altered white matter integrity in anterior thalamic radiation highly associated with PFC (23), and less cortical thickness in PFC (19). These neuroimaging studies proposed that the role of prefrontal cortical structures in BQ addiction, which plays an important role in cognitive behavioral and emotional changes in various kinds of addiction (24)(25)(26)(27).…”

Section: Introductionmentioning

confidence: 99%

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Dysfunction of the Prefrontal Cortex in Betel-Quid–Dependent Chewers

et al. 2020

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Betel quid is the fourth most popular psychoactive agent worldwide. Imaging studies have found altered brain structure in prefrontal cortex (PFC) in betel-quid dependent (BQD) chewers. However, the brain function in PFC associated with BQ use still remains unclear. The present study aimed to examine brain functional activity in PFC in individuals with BQD. This study recruited 48 participants with BQD and 22 normal controls (NCs). Both BQ-specific cue reactivity and Go/NoGo tasks were administered with functional magnetic resonance imaging (fMRI). Behavioral results showed a deficit in the choice reaction time task in BQD group. The fMRI results of the cue reactivity task suggested that, individuals with BQD exhibited responses in right ventromedial PFC, left posterior cingulate cortex (PCC), left lateral parietal lobe (LPL), left middle temporal gyrus and left visual cortex, when seeing BQ images compared with control images. In the Go/NoGo task, relative to NCs group, individuals with BQD showed higher activity in right dorsolateral PFC, right PCC and bilateral LPL between NoGo and Go trials. Across these two tasks, we consistently found disrupted function in PFC in individuals with BQD, which might lead to impaired craving and response inhibition in BQ addiction. Results of current study might shed light on the neural mechanisms involved in BQ use, which could be used as potential guidelines for diagnosis and treatment of BQ dependence.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Dysfunction of the Prefrontal Cortex in Betel-Quid–Dependent Chewers

et al. 2020

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“…The dlPFC also participates in memory processing (58,59), executive functions (60), and decision making (61,62). A previous study has reported that CT of the dlPFC participated in mediating executive function deficits in individuals with BQD (41). The dlPFC has also been linked with cue-induced craving in substance use disorders (63) emanating from drug-related memories (42) that influence reward-related decision making (64).…”

Section: Discussionmentioning

confidence: 99%

“…In one study, individuals with BQD exhibited reduced CT of the dlPFC compared to HC. The observed CT alterations in the dlPFC mediated executive function deficit in BQ dependent individuals (41).…”

Section: Introductionmentioning

confidence: 88%

Reduced Cortical Thickness in the Right Caudal Middle Frontal Is Associated With Symptom Severity in Betel Quid-Dependent Chewers

Sariah

Zhang

et al. 2020

Front. Psychiatry

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Background: Findings from brain structural imaging studies on betel quid dependence have supported relations between betel quid chewing and alterations in gray matter volume and white matter integrity. However, the effect of betel quid chewing on cortical thickness and the link between cortical thickness and symptom severity remains unascertained. Methods: In this observational study, we compared cortical thickness measures from 24 male betel quid-dependent chewers with 27 male healthy controls. Using FreeSufer, we obtained three-dimensional T1-weighted images that were used to compute the thickness of the cerebral cortex throughout the cortical layer. Results: Compared to healthy controls, betel quid dependent chewers displayed significant decreased cortical thickness in the precuneus, entorhinal, right paracentral, middle temporal, and caudal middle frontal gyri. Betel quid dependence scale scores negatively correlated (r =-0.604; p = 0.002) with reduced cortical thickness in the right caudal middle frontal of betel quid-dependent chewers. Conclusion: The findings provide evidence for cortical thickness abnormality in betel dependent chewers and further propose that the severity of betel quid symptoms may be a critical aspect associated with the cortical alterations. The observed alterations may serve as potential mechanisms to explain why BQ chewing behavior is persistent among individuals with betel quid dependence.

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Arecoline induces neurotoxicity in HT22 cells via the promotion of endoplasmic reticulum stress and downregulation of the Nrf2/HO‐1 pathway

Yan,

Ding,

et al. 2024

Environmental Toxicology

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Arecoline, the predominant bioactive substance extracted from areca nut (AN), is the world's fourth most frequently used psychoactive material. Research has revealed that chewing AN can affect the central nervous system (CNS) and may lead to neurocognitive deficits that are possibly linked to the action of arecoline. However, the mechanism behind the neurotoxicity caused by arecoline remains unclear. This study aimed to investigate the neurotoxic effects of arecoline and its underlying mechanism. The results showed that arecoline caused cytotoxicity against HT22 cells in a dose‐dependent manner and induced apoptosis by upregulating the expression of pro‐apoptotic caspase and Bcl‐2 family proteins. Furthermore, arecoline escalated intracellular reactive oxygen species (ROS) levels and Ca2+ concentration with increasing doses, thereby motivating endoplasmic reticulum stress (ERS) and ERS‐associated apoptotic protein expression. Additionally, the study found that arecoline attenuates intracellular antioxidant defense by inhibiting the translocation of NF‐E2‐related factor‐2 (Nrf2) into the nucleus and decreasing downstream Heme oxygenase‐1 (HO‐1) levels. The specific inhibitor Sodium 4‐phenylbutyrate (4‐PBA) can dramatically attenuate arecoline‐mediated cell apoptosis and ERS‐associated apoptotic pathway expression by blocking ERS. The antioxidant N‐Acetylcysteine (NAC) also effectively reverses the arecoline‐mediated increase of ERS‐related apoptotic pathway protein levels by scavenging intracellular ROS accumulation. In conclusion, this study suggests that arecoline induces neurotoxicity in HT22 cells via ERS mediated by oxidative stress‐ and Ca2+ disturbance, as well as by downregulation of the Nrf2/HO‐1 pathway.

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Executive function deficit in betel-quid-dependent chewers: Mediating role of prefrontal cortical thickness

Cited by 12 publications

References 90 publications

Dysfunction of the Prefrontal Cortex in Betel-Quid–Dependent Chewers

Dysfunction of the Prefrontal Cortex in Betel-Quid–Dependent Chewers

Reduced Cortical Thickness in the Right Caudal Middle Frontal Is Associated With Symptom Severity in Betel Quid-Dependent Chewers

Arecoline induces neurotoxicity in HT22 cells via the promotion of endoplasmic reticulum stress and downregulation of the Nrf2/HO‐1 pathway

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