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Cells
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Ageing and Neurodegenerative Diseases, Second Edition
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Ageing and Neurodegenerative Diseases, Second Edition

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 6566

Special Issue Editors

Dr. Feng Wang

E-Mail Website1 Website2
Guest Editor
Department of Human Genetics, Emory University School of Medicine, Atlanta, GA, USA
Interests: non-coding RNA (miRNAs, circRNAs); age-related neurodegenerative diseases (Alzheimer’s disease); epigenetics (5hmc, 5mc, 6mA)
Special Issues, Collections and Topics in MDPI journals
Dr. Antonella Caccamo

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy
Interests: Alzheimer's disease; neurodegeneration; mTOR; necroptosis; transgenic mice
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

AD and diabetes are two age-related diseases, and some studies have shown patients with diabetes to have an increasing risk of developing AD compared with those without the disease. For example, type 2 diabetes (T2D) patients have been observed to have reduced grey matter, white matter, hippocampus, and whole-brain volumes compared with healthy individuals. Although impaired insulin signaling has been found to be a key component of AD pathology and a hallmark of diabetes, the mechanistic pathway that links these two diseases is still not fully understood.

This Special Issue will accept original articles and reviews in the field of neurodegenerative disease. It also welcomes studies investigating age-related diseases’ complex interactions, potential disease biomarkers, and novel drug therapies. Manuscripts focusing on noncoding RNAs in neurodegenerative disease and the underlying biological mechanisms are particularly sought-after.

Dr. Feng Wang
Dr. Antonella Caccamo
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • ageing
  • miRNAs
  • lncRNA
  • circRNAs
  • diabetes
  • neurodegenerative disease
  • insulin signaling

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Related Special Issue

Published Papers (3 papers)

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Research

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19 pages, 3243 KB  
Article
PF-04691502, a PI3K/mTOR Dual Inhibitor, Ameliorates AD-like Pathology in a Mouse Model of AD
by Marika Lanza, Rossella Basilotta, Antonella Caccamo, Giovanna Casili, Alberto Repici, Salvatore Oddo and Emanuela Esposito
Cells 2025, 14(18), 1474; https://doi.org/10.3390/cells14181474 - 21 Sep 2025
Viewed by 725
Abstract
Alzheimer’s disease (AD) is a neurodegenerative disorder that significantly impacts the lives of patients and their families. The pathological features of AD include the accumulation of amyloid-β (Aβ) and Tau, which disrupt neuronal function and communication, ultimately leading to neuronal loss and brain [...] Read more.
Alzheimer’s disease (AD) is a neurodegenerative disorder that significantly impacts the lives of patients and their families. The pathological features of AD include the accumulation of amyloid-β (Aβ) and Tau, which disrupt neuronal function and communication, ultimately leading to neuronal loss and brain atrophy. Efforts to understand the molecular mechanisms underlying these pathological changes have led to advancements in diagnostic techniques and potential therapeutic interventions. However, the complexity of AD necessitates further research to develop more effective treatments and, ideally, preventive measures. Extensive research suggests that diminishing mTOR signaling increases lifespan and health span across various species. Increased PI3K/mTOR signaling has been linked to the progression of AD pathology, leading to neuronal degeneration and impairments in cognitive function. In this study, we explored the therapeutic potential of PF-04691502, a dual PI3K/mTOR inhibitor, in Alzheimer’s disease (AD)-like pathology using male and female B6.Cg-Tg(APPswe, PSEN1dE9)85Dbo/Mmjax mice (APP/PS1), a well-established transgenic model of AD. Eighteen-month-old APP/PS1 and wild-type mice received oral administration of PF-04691502 at a dose of 1 mg/kg for 12 weeks. Following the treatment period, spatial learning and memory were evaluated using the Morris water maze. Subsequently, the mice brains were collected for neuropathological and biochemical assessments. Our findings showed that PF-04691502 enhanced cognitive performance in APP/PS1 mice and significantly reduced insoluble Aβ accumulation in the brain. Mechanistically, these effects were associated with enhanced autophagy induction. Treatment with PF-04691502 increased the LC3-II/LC3-I ratio, upregulated Beclin-1, and elevated LAMP-2 levels, indicative of stimulated autophagosome formation and lysosomal activity. Overall, these preclinical results suggest that PF-04691502 holds promise as a potential therapeutic agent for AD and other aging-related neurodegenerative diseases involving mTOR pathway dysregulation. Full article
(This article belongs to the Special Issue Ageing and Neurodegenerative Diseases, Second Edition)
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18 pages, 3083 KB  
Article
Hypergravity and ERK Inhibition Combined Synergistically Reduce Pathological Tau Phosphorylation in a Neurodegenerative Cell Model
by Valerio Mignucci, Ivana Barravecchia, Davide De Luca, Giacomo Siano, Cristina Di Primio, Jack J. W. A. van Loon and Debora Angeloni
Cells 2025, 14(14), 1058; https://doi.org/10.3390/cells14141058 - 10 Jul 2025
Viewed by 797
Abstract
This study evaluates the effects of hypergravity (HG) on a neurodegenerative model in vitro, looking at how HG influences Tau protein aggregation in Mouse Hippocampal Neuronal Cells (HT22) induced by neurofibrillary tangle seeds. Overall, 50× g significantly, synergistically, reduced the Tau aggregate Area [...] Read more.
This study evaluates the effects of hypergravity (HG) on a neurodegenerative model in vitro, looking at how HG influences Tau protein aggregation in Mouse Hippocampal Neuronal Cells (HT22) induced by neurofibrillary tangle seeds. Overall, 50× g significantly, synergistically, reduced the Tau aggregate Area when combined with ERK-inhibitor PD-0325901, correlating with decreased phosphorylation at critical residues pS262 and pS396. These findings suggest HG treatments may help mitigate cytoskeletal damage linked to Tau aggregation. Full article
(This article belongs to the Special Issue Ageing and Neurodegenerative Diseases, Second Edition)
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Review

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58 pages, 1209 KB  
Review
Age-Related Neurodegenerative Diseases: A Stem Cell’s Perspective
by Belén Calvo, Pierre Schembri-Wismayer and María Beatriz Durán-Alonso
Cells 2025, 14(5), 347; https://doi.org/10.3390/cells14050347 - 27 Feb 2025
Cited by 2 | Viewed by 3092
Abstract
Neurodegenerative diseases encompass a number of very heterogeneous disorders, primarily characterized by neuronal loss and a concomitant decline in neurological function. Examples of this type of clinical condition are Alzheimer’s Disease, Parkinson’s Disease, Huntington’s Disease and Amyotrophic Lateral Sclerosis. Age has been identified [...] Read more.
Neurodegenerative diseases encompass a number of very heterogeneous disorders, primarily characterized by neuronal loss and a concomitant decline in neurological function. Examples of this type of clinical condition are Alzheimer’s Disease, Parkinson’s Disease, Huntington’s Disease and Amyotrophic Lateral Sclerosis. Age has been identified as a major risk in the etiology of these disorders, which explains their increased incidence in developed countries. Unfortunately, despite continued and intensive efforts, no cure has yet been found for any of these diseases; reliable markers that allow for an early diagnosis of the disease and the identification of key molecular events leading to disease onset and progression are lacking. Altered adult neurogenesis appears to precede the appearance of severe symptoms. Given the scarcity of human samples and the considerable differences with model species, increasingly complex human stem-cell-based models are being developed. These are shedding light on the molecular alterations that contribute to disease development, facilitating the identification of new clinical targets and providing a screening platform for the testing of candidate drugs. Moreover, the secretome and other promising features of these cell types are being explored, to use them as replacement cells of high plasticity or as co-adjuvant therapy in combinatorial treatments. Full article
(This article belongs to the Special Issue Ageing and Neurodegenerative Diseases, Second Edition)
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