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Breakthroughs in Diagnostic Prediction and Fundamental Therapeutics of Dementia and Movement Disorders

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (25 March 2024) | Viewed by 5928

Special Issue Editors

Dr. Ichiro Kawahata

E-Mail Website
Guest Editor
Department of CNS Drug Innovation, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai 980-8578, Japan
Interests: CaMKII; neuropsychiatry disorders; drug addiction; neuroinflammation; dementia
Special Issues, Collections and Topics in MDPI journals
Dr. Yasemin M. Akay

E-Mail Website
Guest Editor
Department of Biomedical Engineering, University of Houston, Houston, TX 77204-5060, USA
Interests: coronary artery disease; stent; noninvasive monitoring; nonlinear dynamics analysis; approximate entropy; 3D co-culture; glioblastoma; astrocytes; tumor microenvironment; PEGDA; addiction; cancer research; data science in medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The increase in patients with dementia and motor dysfunction due to the global aging population is a significant social problem. No fundamental treatment for these cognitive-motor disorders has yet been developed. Therefore, understanding the etiology of aging-related disorders and exploring unique therapeutic targets to develop total therapies are urgent issues. Accordingly, comprehending the degeneration of brain function with aging is essential. To this end, it is necessary to distinguish the molecular mechanisms required to maintain neuronal homeostasis and the characteristics of pathogenic proteins. Thus, this Special Issue focuses on the pathogenic mechanism involved in the etiology of neurodegeneration, which includes Alzheimer’s disease (AD), Parkinson’s (PD), and dementia with Lewy bodies (DLB), demonstrating the physiological significance of the pathogenic proteins. We also focus on the disease-related biomarkers associated with the age- and disease-induced loss of neuronal homeostasis. The goal of this Special Issue is to subsequently improve our understanding of aging-related neurodegenerative disorders and to make breakthroughs in the prediction of pathogenesis and the development of fundamental treatments for these diseases.

Potential topics include, but are not limited to: Parkinson’s disease (PD), Dementia with Lewy bodies (DLB), Alzheimer’s disease (AD), pathogenic proteins in the above diseases, biomarkers for AD, PD, and DLB, therapeutic targets and drugs for AD, PD, and DLB, and reviews and future perspectives on the above topics.

Dr. Ichiro Kawahata
Dr. Yasemin M. Akay
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Parkinson’s disease
  • dementia with Lewy bodies
  • Alzheimer’s disease
  • pathogenic protein
  • biomarker
  • therapeutic target
  • drug

Published Papers (4 papers)

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Research

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21 pages, 5118 KiB  
Article
Difference of Cerebrospinal Fluid Biomarkers and Neuropsychiatric Symptoms Profiles among Normal Cognition, Mild Cognitive Impairment, and Dementia Patient
by Ching-Chi Hsu, Shiow-Ing Wang, Hong-Chun Lin, Eric S. Lin, Fan-Pei Yang, Ching-Mao Chang and James Cheng-Chung Wei
Int. J. Mol. Sci. 2024, 25(7), 3919; https://doi.org/10.3390/ijms25073919 - 31 Mar 2024
Viewed by 1557
Abstract
The delineation of biomarkers and neuropsychiatric symptoms across normal cognition, mild cognitive impairment (MCI), and dementia stages holds significant promise for early diagnosis and intervention strategies. This research investigates the association of neuropsychiatric symptoms, evaluated via the Neuropsychiatric Inventory (NPI), with cerebrospinal fluid [...] Read more.
The delineation of biomarkers and neuropsychiatric symptoms across normal cognition, mild cognitive impairment (MCI), and dementia stages holds significant promise for early diagnosis and intervention strategies. This research investigates the association of neuropsychiatric symptoms, evaluated via the Neuropsychiatric Inventory (NPI), with cerebrospinal fluid (CSF) biomarkers (Amyloid-β42, P-tau, T-tau) across a spectrum of cognitive states to enhance diagnostic accuracy and treatment approaches. Drawing from the National Alzheimer’s Coordinating Center’s Uniform Data Set Version 3, comprising 977 individuals with normal cognition, 270 with MCI, and 649 with dementia. To assess neuropsychiatric symptoms, we employed the NPI to understand the behavioral and psychological symptoms associated with each cognitive category. For the analysis of CSF biomarkers, we measured levels of Amyloid-β42, P-tau, and T-tau using the enzyme-linked immunosorbent assay (ELISA) and Luminex multiplex xMAP assay protocols. These biomarkers are critical in understanding the pathophysiological underpinnings of Alzheimer’s disease and its progression, with specific patterns indicative of disease stage and severity. This study cohort consists of 1896 participants, which is composed of 977 individuals with normal cognition, 270 with MCI, and 649 with dementia. Dementia is characterized by significantly higher NPI scores, which are largely reflective of mood-related symptoms (p < 0.001). In terms of biomarkers, normal cognition shows median Amyloid-β at 656.0 pg/mL, MCI at 300.6 pg/mL, and dementia at 298.8 pg/mL (p < 0.001). Median P-tau levels are 36.00 pg/mL in normal cognition, 49.12 pg/mL in MCI, and 58.29 pg/mL in dementia (p < 0.001). Median T-tau levels are 241.0 pg/mL in normal cognition, 140.6 pg/mL in MCI, and 298.3 pg/mL in dementia (p < 0.001). Furthermore, the T-tau/Aβ-42 ratio increases progressively from 0.058 in the normal cognition group to 0.144 in the MCI group, and to 0.209 in the dementia group (p < 0.001). Similarly, the P-tau/Aβ-42 ratio also escalates from 0.305 in individuals with normal cognition to 0.560 in MCI, and to 0.941 in dementia (p < 0.001). The notable disparities in NPI and CSF biomarkers among normal, MCI and Alzheimer’s patients underscore their diagnostic potential. Their combined assessment could greatly improve early detection and precise diagnosis of MCI and dementia, facilitating more effective and timely treatment strategies. Full article
(This article belongs to the Special Issue Breakthroughs in Diagnostic Prediction and Fundamental Therapeutics of Dementia and Movement Disorders)
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12 pages, 3539 KiB  
Article
Using Fatty Acid-Binding Proteins as Potential Biomarkers to Discriminate between Parkinson’s Disease and Dementia with Lewy Bodies: Exploration of a Novel Technique
by Ichiro Kawahata, Tomoki Sekimori, Hideki Oizumi, Atsushi Takeda and Kohji Fukunaga
Int. J. Mol. Sci. 2023, 24(17), 13267; https://doi.org/10.3390/ijms241713267 - 26 Aug 2023
Cited by 3 | Viewed by 2103
Abstract
An increase in the global aging population is leading to an increase in age-related conditions such as dementia and movement disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and dementia with Lewy bodies (DLB). The accurate prediction of risk factors associated with these [...] Read more.
An increase in the global aging population is leading to an increase in age-related conditions such as dementia and movement disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and dementia with Lewy bodies (DLB). The accurate prediction of risk factors associated with these disorders is crucial for early diagnosis and prevention. Biomarkers play a significant role in diagnosing and monitoring diseases. In neurodegenerative disorders like α-synucleinopathies, specific biomarkers can indicate the presence and progression of disease. We previously demonstrated the pathogenic impact of fatty acid-binding proteins (FABPs) in α-synucleinopathies. Therefore, this study investigated FABPs as potential biomarkers for Lewy body diseases. Plasma FABP levels were measured in patients with AD, PD, DLB, and mild cognitive impairment (MCI) and healthy controls. Plasma FABP3 was increased in all groups, while the levels of FABP5 and FABP7 tended to decrease in the AD group. Additionally, FABP2 levels were elevated in PD. A correlation analysis showed that higher FABP3 levels were associated with decreased cognitive function. The plasma concentrations of Tau, GFAP, NF-L, and UCHL1 correlated with cognitive decline. A scoring method was applied to discriminate between diseases, demonstrating high accuracy in distinguishing MCI vs. CN, AD vs. DLB, PD vs. DLB, and AD vs. PD. The study suggests that FABPs could serve as potential biomarkers for Lewy body diseases and aid in early disease detection and differentiation. Full article
(This article belongs to the Special Issue Breakthroughs in Diagnostic Prediction and Fundamental Therapeutics of Dementia and Movement Disorders)
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Review

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21 pages, 5219 KiB  
Review
Alzheimer’s Amyloid Hypothesis and Antibody Therapy: Melting Glaciers?
by Poul F. Høilund-Carlsen, Abass Alavi, Rudolph J. Castellani, Rachael L. Neve, George Perry, Mona-Elisabeth Revheim and Jorge R. Barrio
Int. J. Mol. Sci. 2024, 25(7), 3892; https://doi.org/10.3390/ijms25073892 - 31 Mar 2024
Viewed by 954
Abstract
The amyloid cascade hypothesis for Alzheimer’s disease is still alive, although heavily challenged. Effective anti-amyloid immunotherapy would confirm the hypothesis’ claim that the protein amyloid-beta is the cause of the disease. Two antibodies, aducanumab and lecanemab, have been approved by the U.S. Food [...] Read more.
The amyloid cascade hypothesis for Alzheimer’s disease is still alive, although heavily challenged. Effective anti-amyloid immunotherapy would confirm the hypothesis’ claim that the protein amyloid-beta is the cause of the disease. Two antibodies, aducanumab and lecanemab, have been approved by the U.S. Food and Drug Administration, while a third, donanemab, is under review. The main argument for the FDA approvals is a presumed therapy-induced removal of cerebral amyloid deposits. Lecanemab and donanemab are also thought to cause some statistical delay in the determination of cognitive decline. However, clinical efficacy that is less than with conventional treatment, selection of amyloid-positive trial patients with non-specific amyloid-PET imaging, and uncertain therapy-induced removal of cerebral amyloids in clinical trials cast doubt on this anti-Alzheimer’s antibody therapy and hence on the amyloid hypothesis, calling for a more thorough investigation of the negative impact of this type of therapy on the brain. Full article
(This article belongs to the Special Issue Breakthroughs in Diagnostic Prediction and Fundamental Therapeutics of Dementia and Movement Disorders)
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18 pages, 510 KiB  
Review
Formulating Treatment to Cure Alzheimer’s Dementia: Approach #2
by Jeffrey Fessel
Int. J. Mol. Sci. 2024, 25(6), 3524; https://doi.org/10.3390/ijms25063524 - 20 Mar 2024
Viewed by 736
Abstract
There are two generic approaches to curing any medical condition. The first one treats every patient for all the known possible causes that contribute to pathogenesis; the second one individualizes potentially curative therapy by only identifying in each separate patient the components of [...] Read more.
There are two generic approaches to curing any medical condition. The first one treats every patient for all the known possible causes that contribute to pathogenesis; the second one individualizes potentially curative therapy by only identifying in each separate patient the components of pathogenesis that are actually operative and treating those. This article adopts the second approach for formulating a cure for Alzheimer’s dementia (AD). The components of AD’s pathogenesis are, in alphabetical order, as follows: circadian rhythm disturbances, depression, diabetes and insulin resistance, dyslipidemia, hypertension, inflammation, metabolic syndrome, mitochondrial dysfunction, nutritional deficiencies, TGF-β deficiency, underweight, vascular abnormalities, and Wnt/β-catenin deficiency. For each component, data are described that show the degree to which its prevalence is higher in patients with mild cognitive impairment (MCI) who did not revert to having normal cognition than in those who did because the former group is the pool of patients in which future AD may develop. Only addressing the components that are present in a particular individual potentially is a curative strategy. Published data indicate that curative therapy requires the number of such components that are addressed to be ≥3. Although structural brain changes cannot be directly addressed, the impaired neural tracts result from many of the reversible causal elements, so correcting them will benefit these tracts. Full article
(This article belongs to the Special Issue Breakthroughs in Diagnostic Prediction and Fundamental Therapeutics of Dementia and Movement Disorders)
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