Altered Brain Activity in Depression of Parkinson’s Disease: A Meta-Analysis and Validation Study

Su, Dongning; Cui, Yusha; Li, Zhu; Chen, Huimin; Fang, Jinping; Ma, Huizi; Zhou, Junhong; Feng, Tao

doi:10.3389/fnagi.2022.806054

Cited by 7 publications

(3 citation statements)

References 54 publications

(64 reference statements)

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“…Altered functional connectivity of ventral striatal subregions and between ventromedial putamen and left middle occipital gyrus provided new insight into neural mechanisms of depression in early PD (Wang et al 2022 ). Recent functional MRI studies characterizing the spontaneous blood–oxygen-level-dependence (BOLD) in the whole brain and multiple brain regions revealed reduction in the resting-state BOLD complexity as an important component in the pathology of DPD (Liu et al 2022 ), and a meta-analysis and validation study demonstrated altered BOLD activity in posterior cingulate gyrus, supplementary motor area and cerebellum in DPD compared to non-depressed ones (Su et al 2022 ).…”

Section: Dpd and Brain Circuit Disturbancesmentioning

confidence: 99%

The pathobiological basis of depression in Parkinson disease: challenges and outlooks

Ka¹

2022

J Neural Transm

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Depression, with an estimated prevalence of about 40% is a most common neuropsychiatric disorder in Parkinson disease (PD), with a negative impact on quality of life, cognitive impairment and functional disability, yet the underlying neurobiology is poorly understood. Depression in PD (DPD), one of its most common non-motor symptoms, can precede the onset of motor symptoms but can occur at any stage of the disease. Although its diagnosis is based on standard criteria, due to overlap with other symptoms related to PD or to side effects of treatment, depression is frequently underdiagnosed and undertreated. DPD has been related to a variety of pathogenic mechanisms associated with the underlying neurodegenerative process, in particular dysfunction of neurotransmitter systems (dopaminergic, serotonergic and noradrenergic), as well as to disturbances of cortico-limbic, striato-thalamic-prefrontal, mediotemporal-limbic networks, with disruption in the topological organization of functional mood-related, motor and other essential brain network connections due to alterations in the blood–oxygen-level-dependent (BOLD) fluctuations in multiple brain areas. Other hypothetic mechanisms involve neuroinflammation, neuroimmune dysregulation, stress hormones, neurotrophic, toxic or metabolic factors. The pathophysiology and pathogenesis of DPD are multifactorial and complex, and its interactions with genetic factors, age-related changes, cognitive disposition and other co-morbidities awaits further elucidation.

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Section: Dpd and Brain Circuit Disturbancesmentioning

confidence: 99%

The pathobiological basis of depression in Parkinson disease: challenges and outlooks

Ka¹

2022

J Neural Transm

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“…This capability has advanced the development of physiological-physical models, which serve as a means to investigate and rehabilitate the brain state in patients, providing a framework for understanding the mechanisms underlying neural restoration. Moreover, several fMRI studies have shown that Parkinson's disease patients exhibit altered blood-oxygen-level dependent (BOLD) functional connectivity (FC) between different anatomical regions of a large-scale brain network [34][35][36][37] . Previous research has shown that mean FCs in areas such as the primary motor cortex, premotor cortex, and supplementary motor areas are attenuated in Parkinson's disease patients as compared to healthy controls (HCs) 38 .…”

Section: Introductionmentioning

confidence: 99%

Push-pull effects of basal ganglia network in Parkinson’s disease inferred by functional MRI

Liu,

Wang,

Jiang

et al. 2024

Preprint

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Deep brain stimulation (DBS) has the potential to ameliorate the motor symptoms associated with Parkinson’s disease, such as bradykinesia, rigidity, and tremor. However, the precise therapeutic mechanism underlying DBS in Parkinson’s disease remains inadequately comprehended, impeding the advancement of personalized DBS treatments. This study introduces a bio-inspired multi-scale brain model driven by blood oxygenation-level-dependent (BOLD) signals to explore the neural mechanisms underlying DBS effects on Parkinson’s disease. The model integrates microscopic neural dynamics with macroscopic brain function, utilizes functional Magnetic Resonance Imaging (fMRI) data to uncover the neural basis behind observed brain functional changes. The experiments include 27 Parkinson’s disease patients and 30 healthy controls. Each Parkinson’s disease patient has been conducted DBS surgery targeted on subthalamic nucleus (STN), and the fMRI data are recorded both during DBS-ON and DBS-OFF conditions. Based on our proposed model structure, we fit all the free coupling parameters within the microscopic cortico-basal ganglia-thalamic circuit (CBTC) to match the subject-specific functional connectivity matrix calculated from the fMRI data of each subject. After model validation, we further conduct a three-step deep exploration based on it. Firstly, it is found that an increase in GABAergic transmission into the thalamus has been associated with the exacerbation of rigidity symptom (p = 0.005**), whereas a reduction in GABAergic projections from interneurons within the cortex to pyramidal neurons has been correlated with an elevation in the severity of bradykinesia (p = 0.023*), indicating a “push” effect in the CBTC to impel the symptom-specific coupling intensity to an abnormal state. Secondly, the elevation of GABAergic signaling from the external globus pallidus to the internal globus pallidus indicate a strong correlation with the amelioration of rigidity symptom (p = 0.026*), while the attenuation of excitatory cortical projections to the STN is significantly associated with the remediation of bradykinesia (p = 0.048*). Lastly, the disparity in coupling strength pre- and post-DBS activation is underscored, implying synaptic coupling alterations found in the second step are induced by STN-DBS, which may reveal DBS has the ability to “pull” abnormal network back to a healthy functional state by the directly or indirectly restoration of the loop synaptic characteristics, therefore, normalizing these synaptic couplings. This work provides a promising approach to explore the intrinsic micro-regulatory mechanisms of DBS by interpreting the macroscopic fMRI information, offering new insights into the “push-pull” network dynamics of the CBTC and their implications for motor symptom-specific changes and treatments in Parkinson’s disease.

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“…Secondly, the etiology of depression is complicated and includes social, genetic and psychological factors (13,14). Previous studies reported that the manifestation and severity of depression are not only affected by factors such as gender, educational level, marital status, and income but also depend on other comorbid conditions including stroke, thyroid problems and Parkinson's disease (PD) (15)(16)(17)(18)(19)(20). Importantly, a single nucleotide variation in the oxoglutarate dehydrogenaselike gene rs2293239 (p.Asn725Ser) was identified as a major genetic predictor of familial depression (21).…”

Section: Introductionmentioning

confidence: 99%

Non-linear association between Mediterranean diet and depressive symptom in U.S. adults: A cross-sectional study

et al. 2022

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The Mediterranean diet (MED), a dietary pattern rich in fruits and vegetables, whole grains, legumes, nuts, fish, and olive oil, has anti-oxidative and anti-inflammatory effects. Although some data suggest that MED adherence is associated with decreased manifestation of depressive symptoms, it remains necessary to further analyze this apparent non-linear association as well as the influence of different factors on the relationship between MED and depression. Here, we investigated associations between the alternate MED (aMED) score and depressive symptom via multivariate logistic regression, weighted generalized additive (GAM) and two-step linear regression models, analyzing data from the 2005–2018 National Health and Nutrition Examination Survey (NHANES). The most important factor relevant to aMED score that contributed to the prevalence of depressive symptom was assessed using random forest. Furthermore, we examined whether the relationship between aMED score and depressive symptom differs by age, race, sex, socioeconomic variables, lifestyle- and health-related variables, and chronic medical conditions, via subgroup analyses. A total of 19,477 participants (20–80 years of age) were included in this cross-sectional study. In crude and adjusted (1–5) multivariate logistic regression models, increased aMED score was noted to associate with non-depressive status, as defined using the Patient Health Questionnaire-9 (P < 0.05). Data analyses via GAM and two-piecewise linear regression revealed a non-linear association between aMED and depressive symptom, which had an inflection point of 3. Random forest results revealed that vegetable score contributes greatest to the relationship between aMED and depressive symptom. Subgroup analyses revealed that aMED score is significantly negatively related with depressive symptom in most different populations (P < 0.05) with the exception of high annual income, diabetes, borderline blood glucose level and Parkinson's disease (PD) (P > 0.05). In conclusion, we observed a non-linear association between aMED score and depressive symptom. Further studies are needed to validate our results.

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Altered Brain Activity in Depression of Parkinson’s Disease: A Meta-Analysis and Validation Study

Cited by 7 publications

References 54 publications

The pathobiological basis of depression in Parkinson disease: challenges and outlooks

The pathobiological basis of depression in Parkinson disease: challenges and outlooks

Push-pull effects of basal ganglia network in Parkinson’s disease inferred by functional MRI

Non-linear association between Mediterranean diet and depressive symptom in U.S. adults: A cross-sectional study

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