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Cells
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Aging and Neurodegeneration: Molecular Insights and Emerging Strategies
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Aging and Neurodegeneration: Molecular Insights and Emerging Strategies

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

Deadline for manuscript submissions: 30 August 2026 | Viewed by 3621

Special Issue Editor

Dr. Piotr Paweł Chmielewski

E-Mail Website1 Website2
Guest Editor
Division of Anatomy, Faculty of Medicine, Wroclaw Medical University, Wrocław, Poland
Interests: biogerontology; biomarkers; geroprotective strategies; inflammation; longevity; molecular mechanisms of neurodegeneration; neuroinflammation; therapeutic interventions

Special Issue Information

Dear Colleagues,

The World Health Organization predicts that by 2050, the number of adults affected by dementia will exceed 150 million globally. This growing prevalence underscores the urgent need for a deeper understanding of the molecular and cellular processes driving neurodegenerative conditions to inform the development of effective therapeutic interventions. Age is the primary risk factor for many neurodegenerative disorders, including Alzheimer’s disease, other dementias, and Parkinson’s disease. These conditions are associated with mechanisms such as impaired mitophagy, oxidative stress, molecular damage, endolysosomal dysfunction, chronic inflammation, and altered intercellular communication mediated by extracellular vesicles. These disruptions contribute to hallmark pathologies, including protein misfolding and aggregation (e.g., amyloid-beta peptide, tau protein, or alpha-synuclein), synaptic dysfunction, and ultimately neuronal loss. While these mechanisms are often studied in isolation, a growing body of evidence reveals that they are interconnected. Understanding these pathways provides opportunities to identify common molecular targets for the development of novel therapeutic strategies. In this Special Issue, we invite contributions that explore the fundamental molecular pathways underlying age-related neurodegeneration, innovative biomarkers for early diagnosis, and novel therapeutic approaches. Submissions focusing on translational research, which is indispensable for bridging the gap between bench and bedside, integrative strategies, and systematic reviews are particularly encouraged.

Dr. Piotr Paweł Chmielewski
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 250 words) can be sent to the Editorial Office for assessment.

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

  • Alzheimer’s disease
  • biomarkers
  • endolysosomal pathway
  • extracellular vesicles
  • inflammation
  • mitophagy
  • neurodegeneration
  • neuroinflammation
  • Parkinson’s disease
  • translational research

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Published Papers (2 papers)

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Research

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22 pages, 4363 KB  
Article
Porphyromonas gingivalis-Lipopolysaccharide Induced Caspase-4 Dependent Noncanonical Inflammasome Activation Drives Alzheimer’s Disease Pathologies
by Ambika Verma, Gohar Azhar, Pankaj Patyal, Xiaomin Zhang and Jeanne Y. Wei
Cells 2025, 14(11), 804; https://doi.org/10.3390/cells14110804 - 30 May 2025
Cited by 4 | Viewed by 2505
Abstract
Chronic periodontitis, driven by the keystone pathogen Porphyromonas gingivalis, has been increasingly associated with Alzheimer’s disease (AD) and AD-related dementias (ADRDs). However, the mechanisms through which P. gingivalis-lipopolysaccharide (LPS)-induced release of neuroinflammatory proteins contribute to the pathogenesis of AD and ADRD [...] Read more.
Chronic periodontitis, driven by the keystone pathogen Porphyromonas gingivalis, has been increasingly associated with Alzheimer’s disease (AD) and AD-related dementias (ADRDs). However, the mechanisms through which P. gingivalis-lipopolysaccharide (LPS)-induced release of neuroinflammatory proteins contribute to the pathogenesis of AD and ADRD remain inadequately understood. Caspase-4, a critical mediator of neuroinflammation, plays a pivotal role in these processes following exposure to P. gingivalis-LPS. In this study, we investigated the mechanistic role of caspase-4 in P. gingivalis-LPS-induced IL-1β production, neuroinflammation, oxidative stress, and mitochondrial alterations in human neuronal and microglial cell lines. Silencing of caspase-4 significantly attenuated IL-1β secretion by inhibiting the activation of the caspase-4-NLRP3-caspase-1-gasdermin D inflammasome pathway, confirming its role in neuroinflammation. Moreover, caspase-4 silencing reduced the activation of amyloid precursor protein and presenilin-1, as well as the secretion of amyloid-β peptides, suggesting a role for caspase-4 in amyloidogenesis. Caspase-4 inhibition also restored the expression of key neuroinflammatory markers, such as total tau, VEGF, TGF, and IL-6, highlighting its central role in regulating neuroinflammatory processes. Furthermore, caspase-4 modulated oxidative stress by regulating reactive oxygen species production and reducing oxidative stress markers like inducible nitric oxide synthase and 4-hydroxynonenal. Additionally, caspase-4 influenced mitochondrial membrane potential, mitochondrial biogenesis, fission, fusion, mitochondrial respiration, and ATP production, all of which were impaired by P. gingivalis-LPS but restored with caspase-4 inhibition. These findings provide novel insights into the role of caspase-4 in P. gingivalis-LPS-induced neuroinflammation, oxidative stress, and mitochondrial dysfunction, demonstrating caspase-4 as a potential therapeutic target for neurodegenerative conditions associated with AD and related dementias. Full article
(This article belongs to the Special Issue Aging and Neurodegeneration: Molecular Insights and Emerging Strategies)
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Review

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17 pages, 939 KB  
Review
Orthobiologics and Peptide Therapy for Central Nervous System Repair in Neurodegenerative Conditions
by Cézar Augusto Alves de Oliveira, Bernardo Scaldini Oliveira, Amanda Scaldini Oliveira, Rafael Duarte de Souza Loduca, Carlos Roberto Massella Junior and Gabriel Silva Santos
Cells 2025, 14(23), 1853; https://doi.org/10.3390/cells14231853 - 25 Nov 2025
Viewed by 722
Abstract
Alzheimer’s disease and Parkinson’s disease remain the most prevalent neurodegenerative disorders associated with aging and continue to lack curative treatments. Their pathophysiology is often multifaceted, encompassing protein aggregation, mitochondrial dysfunction, chronic neuroinflammation, synaptic degeneration, and vascular compromise. This complex landscape reduces the effectiveness [...] Read more.
Alzheimer’s disease and Parkinson’s disease remain the most prevalent neurodegenerative disorders associated with aging and continue to lack curative treatments. Their pathophysiology is often multifaceted, encompassing protein aggregation, mitochondrial dysfunction, chronic neuroinflammation, synaptic degeneration, and vascular compromise. This complex landscape reduces the effectiveness of single-target pharmacological agents and underscores the need for therapies capable of acting across multiple axes. Orthobiologics and peptide-based strategies exemplify this approach. Autologous cellular alternatives such as platelet-rich plasma, bone marrow aspirates, mesenchymal stromal cell derivatives, and extracellular vesicles deliver paracrine signals that can reprogram glia, preserve mitochondrial function, and promote synaptic and vascular repair. Peptide therapeutics, including glucagon-like peptide-1 receptor agonists and novel sequences targeting protein aggregation or mitochondrial pathways, provide complementary precision by engaging defined receptors and intracellular cascades. Together, these modalities converge on mechanisms central to circuit preservation rather than symptomatic relief alone. Preclinical studies across Alzheimer’s and Parkinson’s disease demonstrate consistent neuroprotective and functional benefits, and early human trials support feasibility and safety. The translational path forward requires standardized preparation, biomarker integration, optimized delivery routes such as intranasal administration, and regulatory frameworks adapted to biologic therapies. This review synthesizes current evidence on orthobiologics and peptides in neurodegeneration, outlines safety and translational considerations, and highlights future directions, including rational combinations and biomarker-driven trials. By uniting the broad signaling capacity of orthobiologics with the precision of peptides, neurology can move beyond symptomatic care toward regenerative strategies that aim to preserve neural circuits and improve long-term outcomes in Alzheimer’s disease and Parkinson’s disease. Full article
(This article belongs to the Special Issue Aging and Neurodegeneration: Molecular Insights and Emerging Strategies)
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