Aquaporin-4 and Cognitive Disorders

Wang, Yifan; Huang, Chuyi; Guo, Qihao; Chu, Hang

doi:10.14336/ad.2021.0731

Cited by 27 publications

(12 citation statements)

References 78 publications

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“…An EEG study with transgenic mice demonstrated a close correlation between neuronal accumulation of synuclein and slowing of brain oscillations and changes in network excitability [22,41]. Studies have shown that the complex interaction between cholinergic and other transmitter systems participates in the pathophysiological mechanism of brain electricity slowing and cognitive decline in neurodegenerative diseases [42][43][44][45][46]. Other studies and our results suggest that QEEG is a valuable tool to assess the electrophysiological changes related to cognitive impairment or dementia [47].…”

Section: Discussionsupporting

confidence: 62%

QEEG Signatures are Associated with Nonmotor Dysfunctions in Parkinson's Disease and Atypical Parkinsonism: An Integrative Analysis

Liu¹,

Huang²,

Deng³

et al. 2023

Aging and disease

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Parkinson's disease (PD) and atypical parkinsonism (AP), including progressive supranuclear palsy (PSP) and multiple system atrophy (MSA), share similar nonmotor symptoms. Quantitative electroencephalography (QEEG) can be used to examine the nonmotor symptoms. This study aimed to characterize the patterns of QEEG and functional connectivity (FC) that differentiate PD from PSP or MSA, and explore the correlation between the differential QEEG indices and nonmotor dysfunctions in PD and AP. We enrolled 52 patients with PD, 31 with MSA, 22 with PSP, and 50 age-matched health controls to compare QEEG indices among specific brain regions. One-way analysis of variance was applied to assess QEEG indices between groups; Spearman's correlations were used to examine the relationship between QEEG indices and nonmotor symptoms scale (NMSS) and mini-mental state examination (MMSE). FCs using weighted phase lag index were compared between patients with PD and those with MSA/PSP. Patients with PSP revealed higher scores on the NMSS and lower MMSE scores than those with PD and MSA, with similar disease duration. The delta and theta powers revealed a significant increase in PSP, followed by PD and MSA. Patients with PD presented a significantly lower slow-to-fast ratio than those with PSP in the frontal region, while patients with PD presented significantly higher EEG-slowing indices than patients with MSA. The frontal slow-to-fast ratio showed a negative correlation with MMSE scores in patients with PD and PSP, and a positive correlation with NMSS in the perception and mood domain in patients with PSP but not in those with PD. Compared to PD, MSA presented enhanced FC in theta and delta bands in the posterior region, while PSP revealed decreased FC in the delta band within the frontaltemporal cortex. These findings suggest that QEEG might be a useful tool for evaluating the nonmotor dysfunctions in PD and AP. Our QEEG results suggested that with similar disease duration, the cortical neurodegenerative process was likely exacerbated in patients with PSP, followed by those with PD, and lastly in patients with MSA.

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Section: Discussionsupporting

confidence: 62%

QEEG Signatures are Associated with Nonmotor Dysfunctions in Parkinson's Disease and Atypical Parkinsonism: An Integrative Analysis

Liu¹,

Huang²,

Deng³

et al. 2023

Aging and disease

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“…Biondi ring tangles, lipofuscin deposits and lipid droplets rich in oleic acid side chains selectively accumulate in the ependymal cells, ultimately leading to the deterioration of the neurogenic niche of the SVZ, further suppressing neurogenesis and destroying striatal and hippocampal function [54]. Aquaporins such as AQP1 expression and CSF secretion were also diminished [122,123]. By using an unbiased proteomic analyses on autopsy tissue from AD, 25 proteins were found to be significantly increased on the lateral ventricle walls, including amyloid-β , indicating abnormalities in the clearance of some toxic molecules and a decrease in CSF turnover around the ependyma in AD pathology [124].…”

Section: Ependymal Cells In Aging and Alzheimer's Diseasementioning

confidence: 99%

Roles of Ependymal Cells in the Physiology and Pathology of the Central Nervous System

Deng¹,

Lin²,

Liu³

et al. 2022

Aging and disease

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Ependymal cells are indispensable components of the central nervous system (CNS). They originate from neuroepithelial cells of the neural plate and show heterogeneity, with at least three types that are localized in different locations of the CNS. As glial cells in the CNS, accumulating evidence demonstrates that ependymal cells play key roles in mammalian CNS development and normal physiological processes by controlling the production and flow of cerebrospinal fluid (CSF), brain metabolism, and waste clearance. Ependymal cells have been attached to great importance by neuroscientists because of their potential to participate in CNS disease progression. Recent studies have demonstrated that ependymal cells participate in the development and progression of various neurological diseases, such as spinal cord injury and hydrocephalus, raising the possibility that they may serve as a potential therapeutic target for the disease. This review focuses on the function of ependymal cells in the developmental CNS as well as in the CNS after injury and discusses the underlying mechanisms of controlling the functions of ependymal cells.

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“…AQP4 is a water channel highly polarised in the astrocytic end-feet fringing perivasculature basal membranes [ 34 ] that regulates tonicity-responsive cross-membrane transport of water [ 38 ]. In physiological conditions, AQP4 is crucial for efficacious glymphatic movement and CSF clearing [ 39 , 40 , 41 ] via transastrocytic bulk flow [ 42 ], as the majority are localised so that APQ4 are connected to adjacent perivascular spaces, enabling CSF flow between this and the cerebral parenchyma [ 15 ]. Here, the admixture of CSF and interstitial fluid (ISF) occurs, which then travels to subarachnoid spaces where the CSF-ISF then infiltrates into the lymphatic or bloodstream vessels [ 42 ].…”

Section: Glymphatic System and Alzheimer’s Diseasementioning

confidence: 99%

“…In physiological conditions, AQP4 is crucial for efficacious glymphatic movement and CSF clearing [ 39 , 40 , 41 ] via transastrocytic bulk flow [ 42 ], as the majority are localised so that APQ4 are connected to adjacent perivascular spaces, enabling CSF flow between this and the cerebral parenchyma [ 15 ]. Here, the admixture of CSF and interstitial fluid (ISF) occurs, which then travels to subarachnoid spaces where the CSF-ISF then infiltrates into the lymphatic or bloodstream vessels [ 42 ]. As a result, this facilitates a drainage/clearance mechanism of the ISF and, notably, the removal of waste products such as Aβ [ 43 ].…”

Section: Glymphatic System and Alzheimer’s Diseasementioning

confidence: 99%

Research Evidence of the Role of the Glymphatic System and Its Potential Pharmacological Modulation in Neurodegenerative Diseases

Verghese

Terry

Natale

et al. 2022

JCM

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The glymphatic system is a unique pathway that utilises end-feet Aquaporin 4 (AQP4) channels within perivascular astrocytes, which is believed to cause cerebrospinal fluid (CSF) inflow into perivascular space (PVS), providing nutrients and waste disposal of the brain parenchyma. It is theorised that the bulk flow of CSF within the PVS removes waste products, soluble proteins, and products of metabolic activity, such as amyloid-β (Aβ). In the experimental model, the glymphatic system is selectively active during slow-wave sleep, and its activity is affected by both sleep dysfunction and deprivation. Dysfunction of the glymphatic system has been proposed as a potential key driver of neurodegeneration. This hypothesis is indirectly supported by the close relationship between neurodegenerative diseases and sleep alterations, frequently occurring years before the clinical diagnosis. Therefore, a detailed characterisation of the function of the glymphatic system in human physiology and disease would shed light on its early stage pathophysiology. The study of the glymphatic system is also critical to identifying means for its pharmacological modulation, which may have the potential for disease modification. This review will critically outline the primary evidence from literature about the dysfunction of the glymphatic system in neurodegeneration and discuss the rationale and current knowledge about pharmacological modulation of the glymphatic system in the animal model and its potential clinical applications in human clinical trials.

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Aquaporin-4 and Cognitive Disorders

Cited by 27 publications

References 78 publications

QEEG Signatures are Associated with Nonmotor Dysfunctions in Parkinson's Disease and Atypical Parkinsonism: An Integrative Analysis

QEEG Signatures are Associated with Nonmotor Dysfunctions in Parkinson's Disease and Atypical Parkinsonism: An Integrative Analysis

Roles of Ependymal Cells in the Physiology and Pathology of the Central Nervous System

Research Evidence of the Role of the Glymphatic System and Its Potential Pharmacological Modulation in Neurodegenerative Diseases

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