Neuroimaging of Anxiety in Parkinson's Disease: A Systematic Review

Carey, Guillaume; Görmezoğlu, Meltem; Jong, Joost J.A. de; Hofman, Paul; Backes, Walter H.; Dujardin, Kathy; Leentjens, Albert F.G.

doi:10.1002/mds.28404

Cited by 92 publications

(83 citation statements)

References 49 publications

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“…Unilateral 6-OHDA injection in the medial forebrain bundle (MFB) led to anxiety-like behavior with a 96% loss of TH in the STR and 87% loss of neurons in the SNc [ 116 ]. In addition, increased immobility time in the tail suspension task was reported in this model [ 117 ]. This anxiogenic phenotype was reversed by 1.5 mg/kg of diazepam, mainly in the low anxiety hemiparkinsonian rats [ 116 ] and by 14 days treatment with etazolate at a dose of 1 mg/kg [ 117 ].…”

Section: Overview Of Neuropsychiatric and Cognitive Deficits In Rodent Models Of Pdmentioning

confidence: 81%

“…In addition, increased immobility time in the tail suspension task was reported in this model [ 117 ]. This anxiogenic phenotype was reversed by 1.5 mg/kg of diazepam, mainly in the low anxiety hemiparkinsonian rats [ 116 ] and by 14 days treatment with etazolate at a dose of 1 mg/kg [ 117 ]. In the same model, the anxiety-like behavior was also present in the open-field test and EPM [ 118 ], and they were alleviated by hesperidine, which also reduced TH positive neurons loss [ 119 ].…”

Section: Overview Of Neuropsychiatric and Cognitive Deficits In Rodent Models Of Pdmentioning

confidence: 81%

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Neuropsychiatric and Cognitive Deficits in Parkinson’s Disease and Their Modeling in Rodents

et al. 2021

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Parkinson’s disease (PD) is associated with a large burden of non-motor symptoms including olfactory and autonomic dysfunction, as well as neuropsychiatric (depression, anxiety, apathy) and cognitive disorders (executive dysfunctions, memory and learning impairments). Some of these non-motor symptoms may precede the onset of motor symptoms by several years, and they significantly worsen during the course of the disease. The lack of systematic improvement of these non-motor features by dopamine replacement therapy underlines their multifactorial origin, with an involvement of monoaminergic and cholinergic systems, as well as alpha-synuclein pathology in frontal and limbic cortical circuits. Here we describe mood and neuropsychiatric disorders in PD and review their occurrence in rodent models of PD. Altogether, toxin-based rodent models of PD indicate a significant but non-exclusive contribution of mesencephalic dopaminergic loss in anxiety, apathy, and depressive-like behaviors, as well as in learning and memory deficits. Gene-based models display significant deficits in learning and memory, as well as executive functions, highlighting the contribution of alpha-synuclein pathology to these non-motor deficits. Collectively, neuropsychiatric and cognitive deficits are recapitulated to some extent in rodent models, providing partial but nevertheless useful options to understand the pathophysiology of non-motor symptoms and develop therapeutic options for these debilitating symptoms of PD.

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Section: Overview Of Neuropsychiatric and Cognitive Deficits In Rodent Models Of Pdmentioning

confidence: 81%

Section: Overview Of Neuropsychiatric and Cognitive Deficits In Rodent Models Of Pdmentioning

confidence: 81%

Neuropsychiatric and Cognitive Deficits in Parkinson’s Disease and Their Modeling in Rodents

et al. 2021

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“…The scores of BAI and BDI in the PD group were significantly higher than those in the HCs group. Anxiety and depressive disorders are common in PD, which are associated with structural and functional changes of multiple brain regions (Schrag and Taddei, 2017;Carey et al, 2021). In PD with mild to moderate depression, cortical thickness of the precuneus cortex was also significantly increased (Zanigni et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Brain Surface Area Alterations Correlate With Gait Impairments in Parkinson’s Disease

Xuan

Wang

Zhang

et al. 2022

Front. Aging Neurosci.

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Parkinson’s disease (PD) is a common neurodegenerative disease with progressive gait, cognition, and overall functional decline. Surface area changes are frequently seen with aging. In neurodegenerative diseases, the changes can be evident with disease progression. The current study aimed to study the regional microstructural alterations using surface-based morphometry to correlate with gait measures of the pace and rhythm domains in PD patients. We hypothesize that specific regional surface changes can be associated with PD gait impairments. Surface analysis might provide a useful tool for assessing PD for functional status and specific motor domains, such as gait in PD, and potentially could serve as an imaging marker in conjunction with other imaging markers. Twenty-seven PD patients and 37 healthy controls were included. The clinical assessment included Mini-Mental State Exanimation, PD motor assessment, clinical gait testing, and objective/quantitative gait assessment. For patients with PD, all motor and gait testing were performed during both OFF and ON medication states. Three Tesla MRI and high-resolution 3D structural images were acquired with an MP-RAGE pulse sequence. Structural image data preprocessing was performed using the DPABISurf toolbox. Clinical characteristics between PD and control group were compared, and correlation between the surface area and behavioral data were analyzed. At the left lateral temporal cortex (LTC) and right inferior parietal cortex (IPC), PD patients have significantly larger surface areas when compared to controls (P < 0.05) using surface-based morphometry. The surface area changes of the left LTC and right IPC were associated with the worse performance of gait assessed by Berg Balance Scale and Timed Up and Go during OFF (P < 0.01). The left LTC area changes significantly correlated with the number of steps, velocity, and the stride length of the pace domain in the ON state. Our findings suggest that PD is associated with a characteristic regional pattern of larger surface area in the left LTC and right IPC. These regional changes were associated with the pace domain of the gait in the ON state. Overall, surface-based analyses might provide a useful tool for assessing PD for functional status and specific motor domains, such as gait in PD, and potentially could serve as an imaging marker.

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“…Though PD is a progressive neurodegenerative disease that is mainly considered a clinically dominant movement disorder, it also has noticeable non-motor symptoms such as psychiatric signs of depression, anxiety, and cognitive impairment, some of which may appear even before the motor ones (Hemmerle et al, 2012;Lindqvist et al, 2012;Lohle et al, 2019;Mendonca et al, 2020;Carey et al, 2021;Hussein et al, 2021;Kwon et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

Cholinergic Receptor Modulation as a Target for Preventing Dementia in Parkinson’s Disease

2021

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Parkinson’s disease (PD) is a neurodegenerative condition characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) in the midbrain resulting in progressive impairment in cognitive and motor abilities. The physiological and molecular mechanisms triggering dopaminergic neuronal loss are not entirely defined. PD occurrence is associated with various genetic and environmental factors causing inflammation and mitochondrial dysfunction in the brain, leading to oxidative stress, proteinopathy, and reduced viability of dopaminergic neurons. Oxidative stress affects the conformation and function of ions, proteins, and lipids, provoking mitochondrial DNA (mtDNA) mutation and dysfunction. The disruption of protein homeostasis induces the aggregation of alpha-synuclein (α-SYN) and parkin and a deficit in proteasome degradation. Also, oxidative stress affects dopamine release by activating ATP-sensitive potassium channels. The cholinergic system is essential in modulating the striatal cells regulating cognitive and motor functions. Several muscarinic acetylcholine receptors (mAChR) and nicotinic acetylcholine receptors (nAChRs) are expressed in the striatum. The nAChRs signaling reduces neuroinflammation and facilitates neuronal survival, neurotransmitter release, and synaptic plasticity. Since there is a deficit in the nAChRs in PD, inhibiting nAChRs loss in the striatum may help prevent dopaminergic neurons loss in the striatum and its pathological consequences. The nAChRs can also stimulate other brain cells supporting cognitive and motor functions. This review discusses the cholinergic system as a therapeutic target of cotinine to prevent cognitive symptoms and transition to dementia in PD.

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Neuroimaging of Anxiety in Parkinson's Disease: A Systematic Review

Cited by 92 publications

References 49 publications

Neuropsychiatric and Cognitive Deficits in Parkinson’s Disease and Their Modeling in Rodents

Neuropsychiatric and Cognitive Deficits in Parkinson’s Disease and Their Modeling in Rodents

Brain Surface Area Alterations Correlate With Gait Impairments in Parkinson’s Disease

Cholinergic Receptor Modulation as a Target for Preventing Dementia in Parkinson’s Disease

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