Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Molecular Pathogenesis and Treatment in Neurodegeneration: Current Evidence and Future Directions

Print Special Issue Flyer
Special Issue Editors
Special Issue Information
Keywords
Published Papers

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 September 2022) | Viewed by 11537

Share This Special Issue

Special Issue Editor

Dr. Virginia Tancredi

E-Mail Website
Guest Editor

Department of Systems Medicine and Centre of Space Biomedicine, University of Rome “Tor Vergata”, 00133 Rome, Italy
Interests: synaptic plasticity; neurophysiology; aging; physical activity and wellness; cognitive perception; sport training; quality of life
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegeneration is a typical pathological condition of aging characterized by synaptic impairment, neuronal death, and cognitive decline. Although the pathophysiological mechanisms have been extensively studied, to date, many questions persist on this topic. The formation of amyloid deposits in specific areas of the brain has been reported to be responsible for neuronal death. However, several events participate in cell apoptosis, including deregulation of calcium homeostasis, neuroinflammation, mitochondrial dysfunction, and oxidative stress. The involvement of multiple cellular and molecular mechanisms hinders the development of strategies to counter and/or diagnose the cognitive decline underlying neurodegenerative diseases. Moreover, in the absence of a direct cause–effect link between potential risk factors and cognitive decline, the development of preventive approaches to minimize the impact of neurodegeneration still requires further investigation. Therefore, this Special Issue aims to gather information regarding the molecular mechanisms underlying neurodegeneration to identify new potential diagnostic, therapeutic, and preventive strategies to counteract cognitive decline.

Prof. Dr. Virginia Tancredi
Guest Editor

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

neurodegeneration
aging
neuronal death
cognitive decline
synaptic impairment
molecular pathogenesis
clinical treatment
diagnostic strategies
preventive approaches

Published Papers (3 papers)

Download All Papers

Research

Jump to: Review

22 pages, 62966 KiB

Open AccessArticle

Detection of Pathological Markers of Neurodegenerative Diseases following Microfluidic Direct Conversion of Patient Fibroblasts into Neurons

by Cristiana Mollinari, Chiara De Dominicis, Leonardo Lupacchini, Luigi Sansone, Davide Caprini, Carlo Massimo Casciola, Ying Wang, Jian Zhao, Massimo Fini, Matteo Russo, Enrico Garaci and Daniela Merlo

Int. J. Mol. Sci. 2022, 23(4), 2147; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23042147 - 15 Feb 2022

Cited by 6 | Viewed by 3442

Abstract

Neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease are clinically diagnosed using neuropsychological and cognitive tests, expensive neuroimaging-based approaches (MRI and PET) and invasive and time-consuming lumbar puncture for cerebrospinal fluid (CSF) sample collection to detect biomarkers. Thus, a rapid, simple and cost-effective approach to more easily access fluids and tissues is in great need. Here, we exploit the chemical direct reprogramming of patient skin fibroblasts into neurons (chemically induced neurons, ciNs) as a novel strategy for the rapid detection of different pathological markers of neurodegenerative diseases. We found that FAD fibroblasts have a reduced efficiency of reprogramming, and converted ciNs show a less complex neuronal network. In addition, ciNs from patients show misfolded protein accumulation and mitochondria ultrastructural abnormalities, biomarkers commonly associated with neurodegeneration. Moreover, for the first time, we show that microfluidic technology, in combination with chemical reprogramming, enables on-chip examination of disease pathological processes and may have important applications in diagnosis. In conclusion, ciNs on microfluidic devices represent a small-scale, non-invasive and cost-effective high-throughput tool for protein misfolding disease diagnosis and may be useful for new biomarker discovery, disease mechanism studies and design of personalised therapies. Full article

(This article belongs to the Special Issue Molecular Pathogenesis and Treatment in Neurodegeneration: Current Evidence and Future Directions)

► Show Figures

Figure 1

Review

Jump to: Research

27 pages, 1058 KiB

Open AccessReview

Current Insights on the Use of Insulin and the Potential Use of Insulin Mimetics in Targeting Insulin Signalling in Alzheimer’s Disease

by Amy Woodfield, Tatiana Gonzales, Erik Helmerhorst, Simon Laws, Philip Newsholme, Tenielle Porter and Giuseppe Verdile

Int. J. Mol. Sci. 2022, 23(24), 15811; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232415811 - 13 Dec 2022

Cited by 3 | Viewed by 1892

Abstract

Alzheimer’s disease (AD) and type 2 diabetes (T2D) are chronic diseases that share several pathological mechanisms, including insulin resistance and impaired insulin signalling. Their shared features have prompted the evaluation of the drugs used to manage diabetes for the treatment of AD. Insulin delivery itself has been utilized, with promising effects, in improving cognition and reducing AD related neuropathology. The most recent clinical trial involving intranasal insulin reported no slowing of cognitive decline; however, several factors may have impacted the trial outcomes. Long-acting and rapid-acting insulin analogues have also been evaluated within the context of AD with a lack of consistent outcomes. This narrative review provided insight into how targeting insulin signalling in the brain has potential as a therapeutic target for AD and provided a detailed update on the efficacy of insulin, its analogues and the outcomes of human clinical trials. We also discussed the current evidence that warrants the further investigation of the use of the mimetics of insulin for AD. These small molecules may provide a modifiable alternative to insulin, aiding in developing drugs that selectively target insulin signalling in the brain with the aim to attenuate cognitive dysfunction and AD pathologies. Full article

(This article belongs to the Special Issue Molecular Pathogenesis and Treatment in Neurodegeneration: Current Evidence and Future Directions)

► Show Figures

Figure 1

43 pages, 1197 KiB

Open AccessReview

Astrocytes as a Therapeutic Target in Alzheimer’s Disease–Comprehensive Review and Recent Developments

by Mateo Rodríguez-Giraldo, Rodrigo E. González-Reyes, Sofía Ramírez-Guerrero, Carlos E. Bonilla-Trilleras, Santiago Guardo-Maya and Mauricio O. Nava-Mesa

Int. J. Mol. Sci. 2022, 23(21), 13630; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232113630 - 07 Nov 2022

Cited by 24 | Viewed by 5435

Abstract

Alzheimer’s disease (AD) is a frequent and disabling neurodegenerative disorder, in which astrocytes participate in several pathophysiological processes including neuroinflammation, excitotoxicity, oxidative stress and lipid metabolism (along with a critical role in apolipoprotein E function). Current evidence shows that astrocytes have both neuroprotective and neurotoxic effects depending on the disease stage and microenvironmental factors. Furthermore, astrocytes appear to be affected by the presence of amyloid-beta (Aβ), with alterations in calcium levels, gliotransmission and proinflammatory activity via RAGE-NF-κB pathway. In addition, astrocytes play an important role in the metabolism of tau and clearance of Aβ through the glymphatic system. In this review, we will discuss novel pharmacological and non-pharmacological treatments focused on astrocytes as therapeutic targets for AD. These interventions include effects on anti-inflammatory/antioxidant systems, glutamate activity, lipid metabolism, neurovascular coupling and glymphatic system, calcium dysregulation, and in the release of peptides which affects glial and neuronal function. According to the AD stage, these therapies may be of benefit in either preventing or delaying the progression of the disease. Full article

(This article belongs to the Special Issue Molecular Pathogenesis and Treatment in Neurodegeneration: Current Evidence and Future Directions)

► Show Figures