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: 31 October 2025 | Viewed by 1851

Special Issue Editor


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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

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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 (2 papers)

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Review

6187 KiB  
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
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
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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
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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
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