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The Molecular and Cellular Mechanisms of Neurodegenerative Diseases, 2nd Edition
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The Molecular and Cellular Mechanisms of Neurodegenerative Diseases, 2nd Edition

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: 20 June 2025 | Viewed by 3710

Special Issue Editor

Dr. Hongjun (Harry) Fu

E-Mail Website
Guest Editor
Department of Neuroscience, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA
Interests: Alzheimer’s disease; frontotemporal lobar degeneration; traumatic brain injury
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases are a group of age-related complex diseases in the central nervous system including Alzheimer’s disease (AD), Parkinson’s disease (PD), frontotemporal lobar degeneration (FTLD), amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD), and prion diseases. They are characterized by protein aggregates in particular cell types and brain regions, selective neuronal loss, neuroinflammation, progressive degeneration of the nervous system, and neurobehavior changes. Over the last decade, our understanding of neurodegenerative dieases has witnessed significant advances, especially at the molecular and cellular levels, although there are no effective therapeutics to prevent or halt these devastating diseases to date.

The goal of this Special Issue is to gain a better understanding of the cellular and molecular mechanisms in the pathogenesis of different neurodegenerative disorders, with a focus on protein homeostasis, unfolded protein response, synaptic dysfunction, neuroinflammation, alterations in brain metabolism, mitochondrial dysfunction, and oxidative stress mechanisms at the molecular and cellular levels.

We would like to invite you to submit original research articles and reviews that focus on, but are not limited to, innovative and important findings that provide a comprehensive view of the molecular mechanisms underlying the pathogenesis of neurodegenerative diseases. Studies involving transcriptomic, proteomic, and metabolomic approaches are encouraged.

Dr. Hongjun (Harry) Fu
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

  • neurodegenerative diseases
  • Alzheimer’s disease (AD)
  • Parkinson’s disease (PD)
  • frontotemporal lobar degeneration (FTLD)
  • amyotrophic lateral sclerosis (ALS)
  • Huntington’s disease (HD)
  • prion diseases
  • cellular and molecular mechanisms
  • omics

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Published Papers (2 papers)

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15 pages, 735 KiB  
Article
Pleiotropic Associations with Alzheimer’s Disease and Physical Activity: Sex Differences and the Effects of Environment
by Yury Loika, Elena Loiko, Irina Culminskaya and Alexander M. Kulminski
Int. J. Mol. Sci. 2024, 25(23), 12571; https://doi.org/10.3390/ijms252312571 - 22 Nov 2024
Abstract
Abstract: Physical activity (PA) is a modifiable factor in mitigating/preventing Alzheimer’s disease (AD). It is crucial to identify the conditions under which PA’s effects on AD risk would be beneficial. This study aims to gain insights into pleiotropic predisposition to AD and [...] Read more.
Abstract: Physical activity (PA) is a modifiable factor in mitigating/preventing Alzheimer’s disease (AD). It is crucial to identify the conditions under which PA’s effects on AD risk would be beneficial. This study aims to gain insights into pleiotropic predisposition to AD and PA within and across sexes and environmental effects. We performed a genome-wide association study (GWAS) of pleiotropic AD-PA associations in individuals (65 years and older) of European ancestry in a US sample (14,628 individuals), for men and women separately and combined, and contrasted them with the UK biobank (204,789 individuals) to elucidate the effects of the environment. Fisher’s method and Wald's test were used for estimating the significance of pleiotropic associations and differences between the samples. We identified genetic markers in 60 loci with significant pleiotropic associations. Of them, 91.7% of loci exhibited antagonistic relationships characterized by a misalignment of the signs of the associations of the same alleles with AD and PA and a correlation between these phenotypes. Only 16.7% of associations were replicated in the UKB. Phosphorylation and the regulation of transcription were identified as more pronounced biological mechanisms of AD-PA pleiotropy in females and males, respectively. Our results demonstrate the intrinsic heterogeneity of AD-PA pleiotropy and suggest that PA should be used as an intervention against AD with caution, after identifying groups of individuals and combinations of gene–environment interactions with beneficial effects. Full article
(This article belongs to the Special Issue The Molecular and Cellular Mechanisms of Neurodegenerative Diseases, 2nd Edition)

Review

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20 pages, 723 KiB  
Review
Molecular Mechanisms Linking Osteoarthritis and Alzheimer’s Disease: Shared Pathways, Mechanisms and Breakthrough Prospects
by Idiongo Okon Umoh, Helton Jose dos Reis and Antonio Carlos Pinheiro de Oliveira
Int. J. Mol. Sci. 2024, 25(5), 3044; https://doi.org/10.3390/ijms25053044 - 6 Mar 2024
Cited by 6 | Viewed by 2959
Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disease mostly affecting the elderly population. It is characterized by cognitive decline that occurs due to impaired neurotransmission and neuronal death. Even though deposition of amyloid beta (Aβ) peptides and aggregation of hyperphosphorylated TAU have been [...] Read more.
Alzheimer’s disease (AD) is a progressive neurodegenerative disease mostly affecting the elderly population. It is characterized by cognitive decline that occurs due to impaired neurotransmission and neuronal death. Even though deposition of amyloid beta (Aβ) peptides and aggregation of hyperphosphorylated TAU have been established as major pathological hallmarks of the disease, other factors such as the interaction of genetic and environmental factors are believed to contribute to the development and progression of AD. In general, patients initially present mild forgetfulness and difficulty in forming new memories. As it progresses, there are significant impairments in problem solving, social interaction, speech and overall cognitive function of the affected individual. Osteoarthritis (OA) is the most recurrent form of arthritis and widely acknowledged as a whole-joint disease, distinguished by progressive degeneration and erosion of joint cartilage accompanying synovitis and subchondral bone changes that can prompt peripheral inflammatory responses. Also predominantly affecting the elderly, OA frequently embroils weight-bearing joints such as the knees, spine and hips leading to pains, stiffness and diminished joint mobility, which in turn significantly impacts the patient’s standard of life. Both infirmities can co-occur in older adults as a result of independent factors, as multiple health conditions are common in old age. Additionally, risk factors such as genetics, lifestyle changes, age and chronic inflammation may contribute to both conditions in some individuals. Besides localized peripheral low-grade inflammation, it is notable that low-grade systemic inflammation prompted by OA can play a role in AD pathogenesis. Studies have explored relationships between systemic inflammatory-associated diseases like obesity, hypertension, dyslipidemia, diabetes mellitus and AD. Given that AD is the most common form of dementia and shares similar risk factors with OA—both being age-related and low-grade inflammatory-associated diseases, OA may indeed serve as a risk factor for AD. This work aims to review literature on molecular mechanisms linking OA and AD pathologies, and explore potential connections between these conditions alongside future prospects and innovative treatments. Full article
(This article belongs to the Special Issue The Molecular and Cellular Mechanisms of Neurodegenerative Diseases, 2nd Edition)
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