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Biomolecules
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Biomarkers and Risk Factors for Neurodegenerative Disease
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Biomarkers and Risk Factors for Neurodegenerative Disease

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biomarkers".

Deadline for manuscript submissions: closed (26 May 2023) | Viewed by 15241

Special Issue Editors

Dr. Nian Xiong

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Guest Editor
Department of Neurology, Wuhan Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China
Interests: Parkinson’s disease; sleep disorders; biomarkers
Dr. Tao Wang

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Guest Editor
Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
Interests: Parkinson’s disease; sleep disorders; neurotoxin
Prof. Dr. Zhentao Zhang

E-Mail Website
Guest Editor
Department of Neurology, Renmin Hospital of Wuhan University, Wuhan 430060, China
Interests: Alzheimer's disease; Parkinson’s disease; exosome

Special Issue Information

Dear Colleagues,

As the burden of neurodegenerative diseases increases with worldwide aging, there is an urgent need for sensitive cognitive biomarkers. The early prevention and diagnosis of neurodegenerative diseases has always been a challenge, and the current detection methods are limited. In previous studies, neurofilament light protein (NfL) and serum albumin ratio (QAlb) in cerebrospinal fluid (CSF) are widely used as biomarkers, which are helpful for the clinical diagnosis of neurodegenerative diseases. Additionally, the increase levels of Aβ and tau proteins are important indicators for the diagnosis of AD, while α-synuclein is a key biological marker for the diagnosis of PD. In addition to biomarkers in body fluids, alterations of the circadian system have also been suggested as biomarkers of neurodegenerative diseases, expanding our understanding of the pathophysiology and facilitating the development of circadian-based novel interventions for neurodegenerative diseases. Biomarkers of neurodegenerative diseases play an important role in improving clinical diagnosis, disease treatment development and monitoring. This Special Issue aims to discuss novel biomarkers and the development of biomarker-based mechanisms or neuroprotective therapies for neurodegenerative diseases.

Dr. Nian Xiong
Dr. Tao Wang
Prof. Dr. Zhentao Zhang
Guest Editors

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Keywords

  • neurodegenerative diseases
  • biomarkers
  • circadian rhythms
  • therapeutic target

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Published Papers (6 papers)

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Research

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16 pages, 1845 KiB  
Article
Adenosine A2A Receptor Up-Regulation Pre-Dates Deficits of Synaptic Plasticity and of Memory in Mice Exposed to Aβ1–42 to Model Early Alzheimer’s Disease
by Cátia R. Lopes, António C. Silva, Henrique B. Silva, Paula M. Canas, Paula Agostinho, Rodrigo A. Cunha and João Pedro Lopes
Biomolecules 2023, 13(8), 1173; https://doi.org/10.3390/biom13081173 - 28 Jul 2023
Cited by 2 | Viewed by 1385
Abstract
The intracerebroventricular (icv) injection of amyloid peptides (Aβ) models Alzheimer’s disease (AD) in mice, as typified by the onset within 15 days of deficits of memory and of hippocampal long-term potentiation (LTP) that are prevented by the blockade of adenosine A2A receptors [...] Read more.
The intracerebroventricular (icv) injection of amyloid peptides (Aβ) models Alzheimer’s disease (AD) in mice, as typified by the onset within 15 days of deficits of memory and of hippocampal long-term potentiation (LTP) that are prevented by the blockade of adenosine A2A receptors (A2AR). Since A2AR overfunction is sufficient to trigger memory deficits, we tested if A2AR were upregulated in hippocampal synapses before the onset of memory deficits to support the hypothesis that A2AR overfunction could be a trigger of AD. Six to eight days after Aβ-icv injection, mice displayed no alterations of hippocampal dependent memory; however, they presented an increased excitability of hippocampal synapses, a slight increase in LTP magnitude in Schaffer fiber-CA1 pyramid synapses and an increased density of A2AR in hippocampal synapses. A2AR blockade with SCH58261 (50 nM) normalized excitability and LTP in hippocampal slices from mice sacrificed 7–8 days after Aβ-icv injection. Fifteen days after Aβ-icv injection, mice displayed evident deficits of hippocampal-dependent memory deterioration, with reduced hippocampal CA1 LTP but no hyperexcitability and a sustained increase in synaptic A2AR, which blockade restored LTP magnitude. This shows that the upregulation of synaptic A2AR precedes the onset of deterioration of memory and of hippocampal synaptic plasticity, supporting the hypothesis that the overfunction of synaptic A2AR could be a trigger of memory deterioration in AD. Full article
(This article belongs to the Special Issue Biomarkers and Risk Factors for Neurodegenerative Disease)
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13 pages, 2953 KiB  
Article
Temporal Dynamic Alterations of Regional Homogeneity in Parkinson’s Disease: A Resting-State fMRI Study
by Kai Li, Yuan Tian, Haibo Chen, Xinxin Ma, Shuhua Li, Chunmei Li, Shaohui Wu, Fengzhi Liu, Yu Du and Wen Su
Biomolecules 2023, 13(6), 888; https://doi.org/10.3390/biom13060888 - 25 May 2023
Cited by 7 | Viewed by 1824
Abstract
Brain activity is time varying and dynamic, even in the resting state. However, little attention has been paid to the dynamic alterations in regional brain activity in Parkinson’s disease (PD). We aimed to test for differences in dynamic regional homogeneity (dReHo) between PD [...] Read more.
Brain activity is time varying and dynamic, even in the resting state. However, little attention has been paid to the dynamic alterations in regional brain activity in Parkinson’s disease (PD). We aimed to test for differences in dynamic regional homogeneity (dReHo) between PD patients and healthy controls (HCs) and to further investigate the pathophysiological meaning of this altered dReHo in PD. We included 57 PD patients and 31 HCs with rs-fMRI scans and neuropsychological examinations. Then, ReHo and dReHo were calculated for all subjects. We compared ReHo and dReHo between PD patients and HCs and then analyzed the associations between altered dReHo variability and clinical/neuropsychological measurements. Support vector machines (SVMs) were also used to assist in differentiating PD patients from HCs using the classification values of dReHo. The results showed that PD patients had increased ReHo in the bilateral medial temporal lobe and decreased ReHo in the right posterior cerebellar lobe, right precentral gyrus, and supplementary motor area, compared with controls. The coefficient of variation (CV) of dReHo was considerably higher in the precuneus in PD patients compared with HCs, and the CV of dReHo in the precuneus was found to be highly associated with HAMD, HAMA, and NMSQ scores. Multiple linear regression analysis controlling for demographic, clinical, and neuropsychiatric variables confirmed the association between altered dReHo and HAMD. Using the leave-one-out cross validation procedure, 98% (p < 0.001) of individuals were properly identified using the SVM classifier. These results provide new evidence for the aberrant resting-state brain activity in the precuneus of PD patients and its role in neuropsychiatric symptoms in PD. Full article
(This article belongs to the Special Issue Biomarkers and Risk Factors for Neurodegenerative Disease)
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22 pages, 3828 KiB  
Article
MAPK Is a Mutual Pathway Targeted by Anxiety-Related miRNAs, and E2F5 Is a Putative Target for Anxiolytic miRNAs
by Javad Amini, Cordian Beyer, Adib Zendedel and Nima Sanadgol
Biomolecules 2023, 13(3), 544; https://doi.org/10.3390/biom13030544 - 16 Mar 2023
Cited by 3 | Viewed by 2124
Abstract
Anxiety-related disorders (ARDs) are chronic neuropsychological diseases and the sixth leading cause of disability in the world. As dysregulation of microRNAs (miRs) are observed in the pathological course of neuropsychiatric disorders, the present study aimed to introduce miRs that underlie anxiety processing in [...] Read more.
Anxiety-related disorders (ARDs) are chronic neuropsychological diseases and the sixth leading cause of disability in the world. As dysregulation of microRNAs (miRs) are observed in the pathological course of neuropsychiatric disorders, the present study aimed to introduce miRs that underlie anxiety processing in the brain. First, we collected the experimentally confirmed anxiety-related miRNAs (ARmiRs), predicted their target transcripts, and introduced critical cellular pathways with key commune hub genes. As a result, we have found nine anxiolytic and ten anxiogenic ARmiRs. The anxiolytic miRs frequently target the mRNA of Acyl-CoA synthetase long-chain family member 4 (Acsl4), AFF4-AF4/FMR2 family member 4 (Aff4), and Krüppel like transcription factor 4 (Klf4) genes, where miR-34b-5p and miR-34c-5p interact with all of them. Moreover, the anxiogenic miRs frequently target the mRNA of nine genes; among them, only two miR (miR-142-5p and miR-218-5p) have no interaction with the mRNA of trinucleotide repeat-containing adaptor 6B (Tnrc6b), and miR-124-3p interacts with all of them where MAPK is the main signaling pathway affected by both anxiolytic and anxiogenic miR. In addition, the anxiolytic miR commonly target E2F transcription factor 5 (E2F5) in the TGF-β signaling pathway, and the anxiogenic miR commonly target Ataxin 1 (Atxn1), WASP-like actin nucleation promoting factor (Wasl), and Solute Carrier Family 17 Member 6 (Slc17a6) genes in the notch signaling, adherence junction, and synaptic vesicle cycle pathways, respectively. Taken together, we conclude that the most important anxiolytic (miR-34c, Let-7d, and miR-17) and anxiogenic (miR-19b, miR-92a, and 218) miR, as hub epigenetic modulators, potentially influence the pathophysiology of anxiety, primarily via interaction with the MAPK signaling pathway. Moreover, the role of E2F5 as a novel putative target for anxiolytic miRNAs in ARDs disorders deserves further exploration. Full article
(This article belongs to the Special Issue Biomarkers and Risk Factors for Neurodegenerative Disease)
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12 pages, 2946 KiB  
Article
Retinal Structure Abnormalities in Parkinson’s Disease and Atypical Parkinsonism
by Xinxin Ma, Shuhua Li, Bodi Zheng, Lei Hu, Huijing Liu, Zheng Wang, Zhaoxia Wang, Haibo Chen and Wen Su
Biomolecules 2023, 13(2), 218; https://doi.org/10.3390/biom13020218 - 23 Jan 2023
Cited by 3 | Viewed by 1890
Abstract
We investigated retinal structure changes in patients with Parkinson’s disease (PD), multiple system atrophy (MSA), progressive supranuclear palsy (PSP), and controls, and explored the value of this method in differential diagnosis. Spectral domain optical coherence tomography (SD-OCT) was used to measure peripapillary retinal [...] Read more.
We investigated retinal structure changes in patients with Parkinson’s disease (PD), multiple system atrophy (MSA), progressive supranuclear palsy (PSP), and controls, and explored the value of this method in differential diagnosis. Spectral domain optical coherence tomography (SD-OCT) was used to measure peripapillary retinal nerve fiber layer (pRNFL) thickness, and macular thickness and volume. PSP patients showed higher temporal pRNFL thickness than PD and MSA patients. Peripapillary RNFL thickness could be used for discriminating PSP from MSA and PD. PD and MSA patients showed retinal thinning in the foveal center circle and nasal inner sectors compared to controls. Macular thickness and volume could be used for discriminating MSA from PD. There were negative correlations between disease duration and OCT parameters in PD, MSA, and PSP, independent of age, sex ratio, and the side of the eye. PD and atypical parkinsonism correlate with specific patterns of retina alterations. OCT could be a biomarker for differential diagnosis and progression evaluation of parkinsonian syndrome. Full article
(This article belongs to the Special Issue Biomarkers and Risk Factors for Neurodegenerative Disease)
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10 pages, 2738 KiB  
Article
Development of a Gastrointestinal-Myoelectrical-Activity-Based Nomogram Model for Predicting the Risk of Mild Cognitive Impairment
by Baichuan Li, Shuming Ji, Anjiao Peng, Na Yang, Xia Zhao, Peimin Feng, Yunwu Zhang and Lei Chen
Biomolecules 2022, 12(12), 1861; https://doi.org/10.3390/biom12121861 - 12 Dec 2022
Cited by 1 | Viewed by 1914
Abstract
Mild cognitive impairment (MCI) is the prodromal stage and an important risk factor of Alzheimer’s disease (AD). Interventions at the MCI stage are significant in reducing the occurrence of AD. However, there are still many obstacles to the screening of MCI, resulting in [...] Read more.
Mild cognitive impairment (MCI) is the prodromal stage and an important risk factor of Alzheimer’s disease (AD). Interventions at the MCI stage are significant in reducing the occurrence of AD. However, there are still many obstacles to the screening of MCI, resulting in a large number of patients going undetected. Given the strong correlation between gastrointestinal function and neuropsychiatric disorders, the aim of this study is to develop a risk prediction model for MCI based on gastrointestinal myoelectrical activity. The Mini-Mental State Examination and electrogastroenterography were applied to 886 participants in western China. All participants were randomly assigned to the training and validation sets in a ratio of 7:3. In the training set, risk variables were screened using LASSO regression and logistic regression, and risk prediction models were built based on nomogram and decision curve analysis, then validation was performed. Eight predictors were selected in the training set, including four electrogastroenterography parameters (rhythm disturbance, dominant frequency and dominant power ratio of gastric channel after meal, and time difference of intestinal channel after meal). The area under the ROC curve for the prediction model was 0.74 in the training set and 0.75 in the validation set, both of which exhibited great prediction ability. Furthermore, decision curve analysis displayed that the net benefit was more desirable when the risk thresholds ranged from 15% to 35%, indicating that the nomogram was clinically usable. The model based on gastrointestinal myoelectrical activity has great significance in predicting the risk of MCI and is expected to be an alternative to scales assessment. Full article
(This article belongs to the Special Issue Biomarkers and Risk Factors for Neurodegenerative Disease)
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Review

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30 pages, 2176 KiB  
Review
APOE Peripheral and Brain Impact: APOE4 Carriers Accelerate Their Alzheimer Continuum and Have a High Risk of Suicide in PM2.5 Polluted Cities
by Lilian Calderón-Garcidueñas, Jacqueline Hernández-Luna, Mario Aiello-Mora, Rafael Brito-Aguilar, Pablo A. Evelson, Rodolfo Villarreal-Ríos, Ricardo Torres-Jardón, Alberto Ayala and Partha S. Mukherjee
Biomolecules 2023, 13(6), 927; https://doi.org/10.3390/biom13060927 - 31 May 2023
Cited by 5 | Viewed by 5178
Abstract
This Review emphasizes the impact of APOE4—the most significant genetic risk factor for Alzheimer’s disease (AD)—on peripheral and neural effects starting in childhood. We discuss major mechanistic players associated with the APOE alleles’ effects in humans to understand their impact from conception through [...] Read more.
This Review emphasizes the impact of APOE4—the most significant genetic risk factor for Alzheimer’s disease (AD)—on peripheral and neural effects starting in childhood. We discuss major mechanistic players associated with the APOE alleles’ effects in humans to understand their impact from conception through all life stages and the importance of detrimental, synergistic environmental exposures. APOE4 influences AD pathogenesis, and exposure to fine particulate matter (PM2.5), manufactured nanoparticles (NPs), and ultrafine particles (UFPs) associated with combustion and friction processes appear to be major contributors to cerebrovascular dysfunction, neuroinflammation, and oxidative stress. In the context of outdoor and indoor PM pollution burden—as well as Fe, Ti, and Al alloys; Hg, Cu, Ca, Sn, and Si UFPs/NPs—in placenta and fetal brain tissues, urban APOE3 and APOE4 carriers are developing AD biological disease hallmarks (hyperphosphorylated-tau (P-tau) and amyloid beta 42 plaques (Aβ42)). Strikingly, for Metropolitan Mexico City (MMC) young residents ≤ 40 y, APOE4 carriers have 4.92 times higher suicide odds and 23.6 times higher odds of reaching Braak NFT V stage versus APOE4 non-carriers. The National Institute on Aging and Alzheimer’s Association (NIA-AA) framework could serve to test the hypothesis that UFPs and NPs are key players for oxidative stress, neuroinflammation, protein aggregation and misfolding, faulty complex protein quality control, and early damage to cell membranes and organelles of neural and vascular cells. Noninvasive biomarkers indicative of the P-tau and Aβ42 abnormal protein deposits are needed across the disease continuum starting in childhood. Among the 21.8 million MMC residents, we have potentially 4 million APOE4 carriers at accelerated AD progression. These APOE4 individuals are prime candidates for early neuroprotective interventional trials. APOE4 is key in the development of AD evolving from childhood in highly polluted urban centers dominated by anthropogenic and industrial sources of pollution. APOE4 subjects are at higher early risk of AD development, and neuroprotection ought to be implemented. Effective reductions of PM2.5, UFP, and NP emissions from all sources are urgently needed. Alzheimer’s Disease prevention ought to be at the core of the public health response and physicians-scientist minority research be supported. Full article
(This article belongs to the Special Issue Biomarkers and Risk Factors for Neurodegenerative Disease)
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