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Molecular and Neuroimaging Biomarkers in Alzheimer’s Disease and Frontotemporal Lobar...
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Molecular and Neuroimaging Biomarkers in Alzheimer’s Disease and Frontotemporal Lobar Degeneration

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neurodegenerative Diseases".

Deadline for manuscript submissions: closed (31 October 2025) | Viewed by 9219

Special Issue Editor

Dr. Rodolfo Gabriel Gatto

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Guest Editor
Department of Neurology, Mayo Clinic, Rochester, MN, USA
Interests: molecular and neuroimaging biomarkers across neurodegenerative diseases

Special Issue Information

Dear Colleagues,

As life expectancy increases, the number of people with dementia is projected to grow exponentially. Nonetheless, new biotechnologies have been focused on improving detection and treatment exposure at early stages. This Special Issue aims to provide the reader with an overview of novel imaging and molecular techniques that could be proven key in investigating this disease. We welcome authors from any related neuroscience or medical fields to contribute original research articles demonstrating novel neuroimaging methods and/or new molecular biomarkers related to the dementia spectrum study. We welcome contributions on subjects related to (but not limited to) basic, translational, or clinical research applying novel biomarkers in the context of this or related diseases. Manuscripts can be submitted through any related sections of this journal.

Dr. Rodolfo Gabriel Gatto
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. Brain Sciences 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 2200 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

  • neuroimaging
  • biomarkers
  • genetic and molecular biology
  • connectomics
  • neuropathology
  • neuropsychological measures
  • dementia
  • preclinical models
  • alzheimer’s disease
  • frontotemporal dementia

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Published Papers (4 papers)

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Research

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17 pages, 1536 KB  
Article
Sex-Dependent Phenotypic and Histomorphometric Biomarkers in the APPswe/PS1dE9/Blg Mouse Model of Alzheimer’s Disease
by Elena Kuzubova, Alexandra Radchenko, Mikhail Pokrovskii, Olesya Shcheblykina, Kirill Chaprov, Arkadii Nesterov, Tatiana Avtina, Vladimir Pokrovskii and Mikhail Korokin
Brain Sci. 2025, 15(11), 1237; https://doi.org/10.3390/brainsci15111237 - 18 Nov 2025
Viewed by 579
Abstract
Background: Sex-related differences significantly impact biomedical research outcomes, yet female subjects are often excluded due to concerns about variability from the estrous cycle. This study aimed to investigate the sex-dependent differences in behavioral phenotypes and amyloid-beta plaque accumulation in the APPswe/PS1dE9/Blg transgenic [...] Read more.
Background: Sex-related differences significantly impact biomedical research outcomes, yet female subjects are often excluded due to concerns about variability from the estrous cycle. This study aimed to investigate the sex-dependent differences in behavioral phenotypes and amyloid-beta plaque accumulation in the APPswe/PS1dE9/Blg transgenic mouse model of Alzheimer’s disease. Methods: Male and female APPswe/PS1dE9/Blg transgenic mice and wild-type (WT) controls were assessed at 7.5 and 10 months of age. A comprehensive behavioral test battery was employed, including the Open Field, Novel Object Recognition, Y-Maze, and Barnes Maze tests. Histological analysis of amyloid plaque was carried out. Results: Female transgenic mice displayed delayed accumulation of Aβ plaques and milder cognitive decline compared with males. At 10 months, plaque load in females corresponded to that of 7.5-month-old males, demonstrating a temporal lag in pathology. Behavioral impairments correlated negatively with cortical plaque burden (r = −0.4964, p = 0.0181), supporting its role as a structural biomarker of disease progression. Conclusions: This study identifies distinct sex-dependent trajectories of behavioral and histomorphometric biomarkers in APPswe/PS1dE9/Blg mice. Females exhibit delayed amyloid pathology and cognitive decline, suggesting intrinsic neuroprotective mechanisms that modulate biomarker expression over time. These findings emphasize the necessity of integrating both sexes in preclinical biomarker research and support the use of morphometric endpoints as translationally relevant indicators of Alzheimer’s disease progression. Full article
(This article belongs to the Special Issue Molecular and Neuroimaging Biomarkers in Alzheimer’s Disease and Frontotemporal Lobar Degeneration)
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Review

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13 pages, 550 KB  
Review
The cGAS–STING Pathway in Dementia: An Emerging Mechanism of Neuroinflammation
by Young Min, Yoon-Seob Lee, Juwon Lee, Da-Young Keum, Joo-Young Gwag, Sung-Min Jeon, Heejin Jo and Sung-Ung Kang
Brain Sci. 2025, 15(11), 1241; https://doi.org/10.3390/brainsci15111241 - 19 Nov 2025
Viewed by 749
Abstract
Dementia is a growing global health concern in aging societies, leading to a progressive decline in cognitive function that severely impairs daily life. Despite the growing burden, effective preventive and therapeutic strategies remain elusive, emphasizing the urgent need for novel interventions. Recent advances [...] Read more.
Dementia is a growing global health concern in aging societies, leading to a progressive decline in cognitive function that severely impairs daily life. Despite the growing burden, effective preventive and therapeutic strategies remain elusive, emphasizing the urgent need for novel interventions. Recent advances underscore the pivotal role of neuroinflammation in dementia pathogenesis, particularly in Alzheimer’s disease (AD). Chronic activation of central nervous system immune cells, particularly microglia, exacerbates neurodegeneration and establishes a self-perpetuating cycle of inflammation and cognitive decline. This review focuses on emerging research exploring the cGAS-STING pathway’s role in dementia, examining its potential as a diagnostic and therapeutic target. The cGAS-STING pathway, integral to innate immune responses, may contribute to the chronic neuroinflammation seen in neurodegenerative diseases. By targeting this pathway, new strategies could mitigate the inflammatory processes that drive neuronal loss, offering a promising avenue for therapeutic development in dementia. Full article
(This article belongs to the Special Issue Molecular and Neuroimaging Biomarkers in Alzheimer’s Disease and Frontotemporal Lobar Degeneration)
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27 pages, 6187 KB  
Review
Looking into Abnormal Co-Expressions of Tau and TDP-43 in the Realm of Mixed Dementia Types: A Double-Punch Scenario
by Hossam Youssef, Carina Weissmann, Gokhan Uruk and Rodolfo Gabriel Gatto
Brain Sci. 2025, 15(7), 716; https://doi.org/10.3390/brainsci15070716 - 3 Jul 2025
Cited by 4 | Viewed by 3044
Abstract
Transactive response DNA-binding protein of 43 kDa (TDP-43) and tau proteins play critical roles in neurodegenerative diseases, particularly frontotemporal lobar degeneration (FTLD) and Alzheimer’s disease (AD). The co-occurrence of TDP-43 and tau pathologies raises questions about their role in disease progression. This review [...] Read more.
Transactive response DNA-binding protein of 43 kDa (TDP-43) and tau proteins play critical roles in neurodegenerative diseases, particularly frontotemporal lobar degeneration (FTLD) and Alzheimer’s disease (AD). The co-occurrence of TDP-43 and tau pathologies raises questions about their role in disease progression. This review explores the simultaneous presence of tau and TDP-43 co-pathologies, emphasizing their molecular interactions and the resultant neuropathological implications. Additionally, we provide representative examples of their clinical presentations, neuroimaging, and neuropathological findings associated with FTLD-TDP and FTLD-tau, emphasizing the need for a comprehensive understanding of these intertwined pathologies. We analyze various clinical scenarios, including argyrophilic grain disease (AGD), primary age-related tauopathy (PART), and limbic predominant age-related TDP-43 encephalopathy (LATE), to elucidate the complex relationship between these proteinopathies. From the literature, the co-occurrence of tau and TDP-43 is linked to more severe and poorer clinical outcomes compared to isolated pathologies. This review underscores the necessity of considering co-pathologies in the context of FTLD, as they may act as accelerators of cognitive decline. This highlights the importance of integrated approaches in diagnosing and treating neurodegenerative conditions characterized by tau and TDP-43 misfolding. Understanding the interplay between these molecular markers is vital for advancing therapeutic strategies for such disorders. Full article
(This article belongs to the Special Issue Molecular and Neuroimaging Biomarkers in Alzheimer’s Disease and Frontotemporal Lobar Degeneration)
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41 pages, 2878 KB  
Review
Modeling Alzheimer’s Disease: A Review of Gene-Modified and Induced Animal Models, Complex Cell Culture Models, and Computational Modeling
by Anna M. Timofeeva, Kseniya S. Aulova and Georgy A. Nevinsky
Brain Sci. 2025, 15(5), 486; https://doi.org/10.3390/brainsci15050486 - 5 May 2025
Cited by 2 | Viewed by 4189
Abstract
Alzheimer’s disease, a complex neurodegenerative disease, is characterized by the pathological aggregation of insoluble amyloid β and hyperphosphorylated tau. Multiple models of this disease have been employed to investigate the etiology, pathogenesis, and multifactorial aspects of Alzheimer’s disease and facilitate therapeutic development. Mammals, [...] Read more.
Alzheimer’s disease, a complex neurodegenerative disease, is characterized by the pathological aggregation of insoluble amyloid β and hyperphosphorylated tau. Multiple models of this disease have been employed to investigate the etiology, pathogenesis, and multifactorial aspects of Alzheimer’s disease and facilitate therapeutic development. Mammals, especially mice, are the most common models for studying the pathogenesis of this disease in vivo. To date, the scientific literature has documented more than 280 mouse models exhibiting diverse aspects of Alzheimer’s disease pathogenesis. Other mammalian species, including rats, pigs, and primates, have also been utilized as models. Selected aspects of Alzheimer’s disease have also been modeled in simpler model organisms, such as Drosophila melanogaster, Caenorhabditis elegans, and Danio rerio. It is possible to model Alzheimer’s disease not only by creating genetically modified animal lines but also by inducing symptoms of this neurodegenerative disease. This review discusses the main methods of creating induced models, with a particular focus on modeling Alzheimer’s disease on cell cultures. Induced pluripotent stem cell (iPSC) technology has facilitated novel investigations into the mechanistic underpinnings of diverse diseases, including Alzheimer’s. Progress in culturing brain tissue allows for more personalized studies on how drugs affect the brain. Recent years have witnessed substantial advancements in intricate cellular system development, including spheroids, three-dimensional scaffolds, and microfluidic cultures. Microfluidic technologies have emerged as cutting-edge tools for studying intercellular interactions, the tissue microenvironment, and the role of the blood–brain barrier (BBB). Modern biology is experiencing a significant paradigm shift towards utilizing big data and omics technologies. Computational modeling represents a powerful methodology for researching a wide array of human diseases, including Alzheimer’s. Bioinformatic methodologies facilitate the analysis of extensive datasets generated via high-throughput experimentation. It is imperative to underscore the significance of integrating diverse modeling techniques in elucidating pathogenic mechanisms in their entirety. Full article
(This article belongs to the Special Issue Molecular and Neuroimaging Biomarkers in Alzheimer’s Disease and Frontotemporal Lobar Degeneration)
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