ReviewInternational journal of molecular sciences2024
Potential Mechanisms of Tunneling Nanotube Formation and Their Role in Pathology Spread in Alzheimer's Disease and Other Proteinopathies.
Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- A new paradigm in Parkinson's disease: kidney-origin α-synuclein pathology driven by PKC signaling and aurothioglucose.Inflammopharmacology · 2026Review
- Context-Dependent Functional Outcomes of Mitochondrial Transfer: A Donor-Recipient Perspective.Advanced biology · 2026Review
- Recent trends in anti-Alzheimer's potential of novel biologically active isatin analogues: synthetic strategies, structural activity relationship studies and molecular docking insights.Molecular diversity · 2026Review
- Advancements in Nanomaterial-Based Biosensors for Neuropsychiatric and Neurodegenerative Diagnostics: From Biomarker Discovery to Clinical Translation.Biosensors · 2026Review
- The molecular architecture of tunneling nanotubes.bioRxiv : the preprint server for biology · 2026Article
- Dysfunction of the CD38-Miro1 Axis Disrupts Astrocyte-neuron Mitochondrial Transfer in Alzheimer's Disease: Mechanisms and Therapeutic Restoration.Journal of molecular neuroscience : MN · 2026Review
- Extracellular Protein Quality Control in Tau Pathology.Molecular neurobiology · 2026Review
- From the energy factory to the intercellular communication medium: the emerging role of intercellular mitochondrial transfer and mitochondrial transplantation therapy in diabetes and diabetic complications.Journal of translational medicine · 2026Review
- Chaetoglobosin F Attenuates Amyloid-β-Induced Neurotoxicity in Caenorhabditis elegans by Regulating Autophagy and Oxidative Stress Via the Insulin/IGF-1 and p38 MAPK Pathways.Neurochemical research · 2026Article
- Mitochondrial Transplantation Therapy for Ischemic Stroke: Progress and Challenges.Cellular and molecular neurobiology · 2026Review
- Tunneling Nanotubes in Astrocyte-Neuron Crosstalk: From Intercellular Communication and Pathological Spread to Mechanobiological and Bio-Inspired Approaches.Brain sciences · 2026Review
- Smart Biosensing Nanomaterials for Alzheimer's Disease: Advances in Design and Drug Delivery Strategies to Overcome the Blood-Brain Barrier.Biosensors · 2026Review
- Nanotubular networks in the aging brain: from neuroprotection to neurodegeneration.Frontiers in human neuroscience · 2026Article
- Nano- and Microtubes: Tiny Fusion Events but Not Overall Plasma Membrane Merger for Exchanging Intracellular Components.Advances in experimental medicine and biology · 2026Review
- Brain rewired: Redox control of brain cell crosstalk via nanotubes and vesicles.Free radical biology & medicine · 2025Review
- Review
- Unraveling the Intricacies: The Role of miRNAs in the Progression and Initiation of Alzheimer's Disease.Current Alzheimer research · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Alzheimer's disease (AD) is the most common type of dementia worldwide. The etiopathogenesis of this disease remains unknown. Currently, several hypotheses attempt to explain its cause, with the most well-studied being the cholinergic, beta-amyloid (Aβ), and Tau hypotheses. Lately, there has been increasing interest in the role of immunological factors and other proteins such as alpha-synuclein (α-syn) and transactive response DNA-binding protein of 43 kDa (TDP-43). Recent studies emphasize the role of tunneling nanotubes (TNTs) in the spread of pathological proteins within the brains of AD patients. TNTs are small membrane protrusions composed of F-actin that connect non-adjacent cells. Conditions such as pathogen infections, oxidative stress, inflammation, and misfolded protein accumulation lead to the formation of TNTs. These structures have been shown to transport pathological proteins such as Aβ, Tau, α-syn, and TDP-43 between central nervous system (CNS) cells, as confirmed by in vitro studies. Besides their role in spreading pathology, TNTs may also have protective functions. Neurons burdened with α-syn can transfer protein aggregates to glial cells and receive healthy mitochondria, thereby reducing cellular stress associated with α-syn accumulation. Current AD treatments focus on alleviating symptoms, and clinical trials with Aβ-lowering drugs have proven ineffective. Therefore, intensifying research on TNTs could bring scientists closer to a better understanding of AD and the development of effective therapies.
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