Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
3.7
4.7
Journals
Biomedicines
Special Issues
Feature Reviews in Neurodegenerative Diseases and Environmental Factors
share announcement

Feature Reviews in Neurodegenerative Diseases and Environmental Factors

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 10054

Special Issue Editor

Dr. Katarína Štroffeková

E-Mail Website
Guest Editor
Department of Biophysics, Faculty of Science, PJ Safarik University, Kosice, Slovakia
Interests: neurodegenerative diseases; mitochondria; oxidative stress; apoptosis; autophagy; Bcl2 proteins; photobiomodulation; Ca2+ channels

Special Issue Information

Dear Colleagues,

The proportion of world population older than 60 years is steadily increasing according to the World Health Organization (WHO). Aging is considered the greatest risk factor for neurodegeneration, therefore prevalence of neurological disorders is expected to rise. The etiology of most neurodegenerative disorders, such as Alzheimer’s and Parkinson’s diseases (AD and PD) and amyotrophic lateral sclerosis (ALS), is multifactorial and consists of an interaction between environmental factors and genetic predisposition. It is widely accepted that oxidative stress, impairment of mitochondrial dynamics and function, calcium overload, and balance disruption between apoptosis and autophagy are between the key mechanisms that underlie above mentioned neurodegenerative disorders. The scope of this Special Issue is to focus on recent advances in understanding of these mechanisms at the cellular and molecular level with respect to impacts of environmental factors such as pesticides, air and water pollution, and micro- and nano-plastics. Reviews regarding these topics are welcome.

Dr. Katarína Štroffeková
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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • neurodegenerative diseases
  • pathophysiology of neurodegeneration
  • oxidative stress
  • apoptosis
  • autophagy
  • mitochondria and Bcl2 proteins
  • endoplasmic reticulum
  • environmental factors – pesticides
  • pollution
  • micro- and nano-plastics
  • neuronal dysfunction and protein aggregation
  • 2D to 3D models for neurodegeneration

Published Papers (5 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Review

20 pages, 2633 KiB  
Review
The Optic Nerve at Stake: Update on Environmental Factors Modulating Expression of Leber’s Hereditary Optic Neuropathy
by Pierre Layrolle, Christophe Orssaud, Maryse Leleu, Pierre Payoux and Stéphane Chavanas
Biomedicines 2024, 12(3), 584; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines12030584 - 6 Mar 2024
Viewed by 890
Abstract
Optic neuropathies are characterized by the degeneration of the optic nerves and represent a considerable individual and societal burden. Notably, Leber’s hereditary optic neuropathy (LHON) is a devastating vision disease caused by mitochondrial gene mutations that hinder oxidative phosphorylation and increase oxidative stress, [...] Read more.
Optic neuropathies are characterized by the degeneration of the optic nerves and represent a considerable individual and societal burden. Notably, Leber’s hereditary optic neuropathy (LHON) is a devastating vision disease caused by mitochondrial gene mutations that hinder oxidative phosphorylation and increase oxidative stress, leading to the loss of retinal ganglion neurons and axons. Loss of vision is rapid and severe, predominantly in young adults. Penetrance is incomplete, and the time of onset is unpredictable. Recent findings revealed that the incidence of genetic LHON susceptibility is around 1 in 1000, much higher than believed till now. Environmental factors are critical in LHON triggering or severity. Families at risk have a very strong demand for how to prevent the onset or limit the severity of the disease. Here, we review recent knowledge of the extrinsic determinants of LHON expression, including lifestyle, dietary supplements, common chemicals, and drugs. Full article
(This article belongs to the Special Issue Feature Reviews in Neurodegenerative Diseases and Environmental Factors)
►▼ Show Figures

Figure 1

30 pages, 891 KiB  
Review
Life Experience Matters: Enrichment and Stress Can Influence the Likelihood of Developing Alzheimer’s Disease via Gut Microbiome
by Sarah E. Torraville, Cassandra M. Flynn, Tori L. Kendall and Qi Yuan
Biomedicines 2023, 11(7), 1884; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines11071884 - 3 Jul 2023
Viewed by 1447
Abstract
Alzheimer’s disease (AD) is a chronic neurodegenerative disease, characterized by the presence of β-amyloid (Aβ) plaques and neurofibrillary tangles (NFTs) formed from abnormally phosphorylated tau proteins (ptau). To date, there is no cure for AD. Earlier therapeutic efforts have focused on the clinical [...] Read more.
Alzheimer’s disease (AD) is a chronic neurodegenerative disease, characterized by the presence of β-amyloid (Aβ) plaques and neurofibrillary tangles (NFTs) formed from abnormally phosphorylated tau proteins (ptau). To date, there is no cure for AD. Earlier therapeutic efforts have focused on the clinical stages of AD. Despite paramount efforts and costs, pharmaceutical interventions including antibody therapies targeting Aβ have largely failed. This highlights the need to alternate treatment strategies and a shift of focus to early pre-clinical stages. Approximately 25–40% of AD cases can be attributed to environmental factors including chronic stress. Gut dysbiosis has been associated with stress and the pathogenesis of AD and can increase both Aβ and NFTs in animal models of the disease. Both stress and enrichment have been shown to alter AD progression and gut health. Targeting stress-induced gut dysbiosis through probiotic supplementation could provide a promising intervention to delay disease progression. In this review, we discuss the effects of stress, enrichment, and gut dysbiosis in AD models and the promising evidence from probiotic intervention studies. Full article
(This article belongs to the Special Issue Feature Reviews in Neurodegenerative Diseases and Environmental Factors)
►▼ Show Figures

Graphical abstract

19 pages, 1348 KiB  
Review
Air Pollution: A Silent Key Driver of Dementia
by Pawel Serafin, Malgorzata Zaremba, Dorota Sulejczak and Patrycja Kleczkowska
Biomedicines 2023, 11(5), 1477; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines11051477 - 18 May 2023
Cited by 3 | Viewed by 2143
Abstract
In 2017, the Lancet Commission on Dementia Prevention, Intervention, and Care included air pollution in its list of potential risk factors for dementia; in 2018, the Lancet Commission on Pollution concluded that the evidence for a causal relationship between fine particulate matter (PM) [...] Read more.
In 2017, the Lancet Commission on Dementia Prevention, Intervention, and Care included air pollution in its list of potential risk factors for dementia; in 2018, the Lancet Commission on Pollution concluded that the evidence for a causal relationship between fine particulate matter (PM) and dementia is encouraging. However, few interventions exist to delay or prevent the onset of dementia. Air quality data are becoming increasingly available, and the science underlying the associated health effects is also evolving rapidly. Recent interest in this area has led to the publication of population-based cohort studies, but these studies have used different approaches to identify cases of dementia. The purpose of this article is to review recent evidence describing the association between exposure to air pollution and dementia with special emphasis on fine particulate matter of 2.5 microns or less. We also summarize here the proposed detailed mechanisms by which air pollutants reach the brain and activate the innate immune response. In addition, the article also provides a short overview of existing limitations in the treatment of dementia. Full article
(This article belongs to the Special Issue Feature Reviews in Neurodegenerative Diseases and Environmental Factors)
►▼ Show Figures

Figure 1

25 pages, 1336 KiB  
Review
Increased Risk of Aging-Related Neurodegenerative Disease after Traumatic Brain Injury
by Sarah Barker, Bindu D. Paul and Andrew A. Pieper
Biomedicines 2023, 11(4), 1154; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines11041154 - 11 Apr 2023
Cited by 8 | Viewed by 2814
Abstract
Traumatic brain injury (TBI) survivors frequently suffer from chronically progressive complications, including significantly increased risk of developing aging-related neurodegenerative disease. As advances in neurocritical care increase the number of TBI survivors, the impact and awareness of this problem are growing. The mechanisms by [...] Read more.
Traumatic brain injury (TBI) survivors frequently suffer from chronically progressive complications, including significantly increased risk of developing aging-related neurodegenerative disease. As advances in neurocritical care increase the number of TBI survivors, the impact and awareness of this problem are growing. The mechanisms by which TBI increases the risk of developing aging-related neurodegenerative disease, however, are not completely understood. As a result, there are no protective treatments for patients. Here, we review the current literature surrounding the epidemiology and potential mechanistic relationships between brain injury and aging-related neurodegenerative disease. In addition to increasing the risk for developing all forms of dementia, the most prominent aging-related neurodegenerative conditions that are accelerated by TBI are amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), Parkinson’s disease (PD), and Alzheimer’s disease (AD), with ALS and FTD being the least well-established. Mechanistic links between TBI and all forms of dementia that are reviewed include oxidative stress, dysregulated proteostasis, and neuroinflammation. Disease-specific mechanistic links with TBI that are reviewed include TAR DNA binding protein 43 and motor cortex lesions in ALS and FTD; alpha-synuclein, dopaminergic cell death, and synergistic toxin exposure in PD; and brain insulin resistance, amyloid beta pathology, and tau pathology in AD. While compelling mechanistic links have been identified, significantly expanded investigation in the field is needed to develop therapies to protect TBI survivors from the increased risk of aging-related neurodegenerative disease. Full article
(This article belongs to the Special Issue Feature Reviews in Neurodegenerative Diseases and Environmental Factors)
►▼ Show Figures

Figure 1

20 pages, 732 KiB  
Review
Gene–Environment Interactions in Repeat Expansion Diseases: Mechanisms of Environmentally Induced Repeat Instability
by Stephanie Calluori, Rebecca Stark and Brandon L. Pearson
Biomedicines 2023, 11(2), 515; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines11020515 - 10 Feb 2023
Cited by 1 | Viewed by 1954
Abstract
Short tandem repeats (STRs) are units of 1–6 base pairs that occur in tandem repetition to form a repeat tract. STRs exhibit repeat instability, which generates expansions or contractions of the repeat tract. Over 50 diseases, primarily affecting the central nervous system and [...] Read more.
Short tandem repeats (STRs) are units of 1–6 base pairs that occur in tandem repetition to form a repeat tract. STRs exhibit repeat instability, which generates expansions or contractions of the repeat tract. Over 50 diseases, primarily affecting the central nervous system and muscles, are characterized by repeat instability. Longer repeat tracts are typically associated with earlier age of onset and increased disease severity. Environmental exposures are suspected to play a role in the pathogenesis of repeat expansion diseases. Here, we review the current knowledge of mechanisms of environmentally induced repeat instability in repeat expansion diseases. The current evidence demonstrates that environmental factors modulate repeat instability via DNA damage and induction of DNA repair pathways, with distinct mechanisms for repeat expansion and contraction. Of particular note, oxidative stress is a key mediator of environmentally induced repeat instability. The preliminary evidence suggests epigenetic modifications as potential mediators of environmentally induced repeat instability. Future research incorporating an array of environmental exposures, new human cohorts, and improved model systems, with a continued focus on cell-types, tissues, and critical windows, will aid in identifying mechanisms of environmentally induced repeat instability. Identifying environmental modulators of repeat instability and their mechanisms of action will inform preventions, therapies, and public health measures. Full article
(This article belongs to the Special Issue Feature Reviews in Neurodegenerative Diseases and Environmental Factors)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-5
Back to TopTop