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Cells
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New Discoveries in Calcium Signaling-Related Neurological Disorders
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New Discoveries in Calcium Signaling-Related Neurological Disorders

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

Deadline for manuscript submissions: 30 April 2026 | Viewed by 6502

Special Issue Editor

Dr. Matheus De Castro Fonseca

E-Mail Website
Guest Editor
Laboratory of Sarkis Mazmanian, Division of Biology and Biological Engineering, California Institute of Technology, 1200 E. California Boulevard, Pasadena, CA 91125, USA
Interests: microbiome; Ca2+ signaling; Parkinson’s disease; protein aggregation; brain physiology

Special Issue Information

Dear Colleagues,

The ubiquitous intracellular messenger calcium (Ca2+) exerts regulatory control over virtually every activity in eukaryotic cells, particularly in excitable cells. Within neurons, Ca2+ assumes a crucial role in the regulation and modulation of essential physiological processes, spanning from synaptic activity to neuronal plasticity. Given the necessity for a highly refined and precise control of Ca2+ levels within specific cellular compartments in neurons, the organizational structure of the Ca2+ signaling machinery in neurons is notably intricate. The malfunctioning of the Ca2+ signaling pathway, which oversees numerous neuronal processes, has been linked to the onset and progression of significant neural disorders in humans. Conditions such as Alzheimer's disease, bipolar disorder, and schizophrenia have been implicated in instances where the Ca2+ signaling pathway experiences dysregulation.

This Special Issue aims to put together all the recent findings on how Ca2+ dysregulation can contribute to the outcome and progression of several neurological disorders.

Dr. Matheus De Castro Fonseca
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

  • Ca2+ signaling
  • neurons
  • neurological disorders
  • intracellular signaling
  • synaptic dysfunction

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Published Papers (4 papers)

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Research

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17 pages, 4541 KB  
Article
Neurophysiological In Vitro Model of Amyloid-β-Induced Deficits of Hippocampal LTP Involving Neuronal Adenosine A2A Receptor Dysfunction Through CD73
by Francisco Q. Gonçalves, Henrique B. Silva, Ângelo R. Tomé, Paula Agostinho, Rodrigo A. Cunha and João P. Lopes
Cells 2026, 15(6), 510; https://doi.org/10.3390/cells15060510 - 13 Mar 2026
Viewed by 237
Abstract
Amyloid-β peptides (Aβ) are considered a main culprit of Alzheimer’s disease (AD), leading to synaptic dysfunction and memory deficits. Although studies in animal models of AD converge to show alterations of synaptic plasticity, namely of long-term potentiation (LTP), the mechanisms through which Aβ [...] Read more.
Amyloid-β peptides (Aβ) are considered a main culprit of Alzheimer’s disease (AD), leading to synaptic dysfunction and memory deficits. Although studies in animal models of AD converge to show alterations of synaptic plasticity, namely of long-term potentiation (LTP), the mechanisms through which Aβ affects synaptic function remain to be unveiled. In this study, we established experimental conditions showing that the acute exposure of mouse hippocampal slices to optimized concentrations of Aβ impaired short-term (PPF-paired-pulse facilitation) and long-term (LTP-long-term potentiation) plasticity without altering basal synaptic transmission. We observed that the elimination of extracellular adenosine with adenosine deaminase abrogated the impact of Aβ on synaptic plasticity, showing a mandatory involvement of extracellular adenosine in the neurophysiological effects of Aβ. Additionally, inhibiting adenosine receptor function with caffeine, as well as selectively blocking adenosine A1 receptors (A1R) with DPCPX, or adenosine A2A receptor (A2AR) with either an antagonist SCH58261 or through knocking out A2AR, demonstrated that acute Aβ modified mouse hippocampal PPF via A1R and LTP through A2AR. Furthermore, the use of slices from mice bearing forebrain-neuron A2AR deletion, along with the application of α,β-methylene ADP, a CD73 inhibitor, confirmed that the neurophysiological actions of Aβ on hippocampal LTP occur selectively through the overfunction of neuronal A2AR via CD73-mediated formation of extracellular adenosine. Overall, the exploitation of a neurophysiological model of early AD, based on the acute administration of Aβ to hippocampal slices, confirmed the critical involvement of adenosine signaling in the impact of Aβ on synaptic plasticity. Full article
(This article belongs to the Special Issue New Discoveries in Calcium Signaling-Related Neurological Disorders)
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Review

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23 pages, 1332 KB  
Review
The Calcium Connection: Explaining Motor Neuron Vulnerability in ALS
by Tristan Dellazizzo Toth, Silvano Bond and Smita Saxena
Cells 2026, 15(4), 322; https://doi.org/10.3390/cells15040322 - 9 Feb 2026
Viewed by 1047
Abstract
ALS is a severe neuromuscular disease classically characterized by the progressive loss of motor neurons, leading to incremental muscle weakness and eventually death. Current treatment options for ALS have proven to have limited effect, merely delaying the progression of symptoms and prolonging patient [...] Read more.
ALS is a severe neuromuscular disease classically characterized by the progressive loss of motor neurons, leading to incremental muscle weakness and eventually death. Current treatment options for ALS have proven to have limited effect, merely delaying the progression of symptoms and prolonging patient survival. This motor neuron subtype-related differential vulnerability has been linked to neuron excitability, metabolism, and protein aggregation. Calcium dysregulation, which serves as an important second messenger in neural signaling pathways, has been implicated in each of these mechanisms and represents a potential target for therapeutic intervention. Armed with cutting-edge tools for visualizing and recording calcium transients in vivo, ALS researchers have delved deeper into the role of calcium dysregulation in disease in recent years. Vulnerable motor neuron populations display an excess of calcium-permeable ion channels together with reduced expression of calcium-binding proteins, generating a cellular environment primed for excitotoxic stress. Loss of inhibitory synaptic input further heightens susceptibility to calcium overload. Paradoxically, some evidence suggests that elevated neuronal activity can exert neuroprotective effects, highlighting the complexity of activity-dependent calcium signaling in ALS. Additionally, ALS-related toxic protein accumulation disrupts calcium homeostasis, contributing to endoplasmic reticulum stress and mitochondrial dysfunction. Emerging data indicate that calcium dysregulation impairs neuron-glia communication, amplifying neuroinflammation and accelerating disease progression. This review aims to synthesize current evidence on how calcium imbalance contributes to motor neuron vulnerability and degeneration in ALS. By exploring the cellular, synaptic, and network-level mechanisms of calcium dysregulation in ALS, the review examines its interplay with mitochondrial and ER stress and explores its impact on neuron-glia interactions with the aim of synthesizing key mechanistic insights into the disease pathogenesis and therapeutic targets. Full article
(This article belongs to the Special Issue New Discoveries in Calcium Signaling-Related Neurological Disorders)
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29 pages, 809 KB  
Review
Endocrine Disorders of Calcium Signaling in Children: Neuroendocrine Crosstalk and Clinical Implications
by Roberto Paparella, Francesca Pastore, Lavinia Marchetti, Arianna Bei, Irene Bernabei, Norma Iafrate, Vittorio Maglione, Marcello Niceta, Anna Zambrano, Mauro Celli, Marco Fiore, Ida Pucarelli and Luigi Tarani
Cells 2026, 15(2), 140; https://doi.org/10.3390/cells15020140 - 13 Jan 2026
Viewed by 1012
Abstract
Calcium ions (Ca2+) serve as universal second messengers regulating endocrine, neuronal, and metabolic processes. In children and adolescents, tight calcium signaling control is crucial for growth, hormone homeostasis, neuromuscular function, and neurodevelopment. Disruptions in Ca2+-dependent pathways—whether genetic, metabolic, or [...] Read more.
Calcium ions (Ca2+) serve as universal second messengers regulating endocrine, neuronal, and metabolic processes. In children and adolescents, tight calcium signaling control is crucial for growth, hormone homeostasis, neuromuscular function, and neurodevelopment. Disruptions in Ca2+-dependent pathways—whether genetic, metabolic, or acquired—underlie a spectrum of pediatric endocrine diseases often presenting with neurological manifestations This review summarizes calcium’s roles in hormone secretion, parathyroid and vitamin D metabolism, and neuronal excitability, and discusses monogenic and metabolic disorders affecting calcium sensing and signaling, including CASR, GNA11, AP2S1, STIM1, and ORAI1 mutations. Diagnostic challenges, therapeutic strategies, and future directions for precision medicine in pediatric neuroendocrinology are highlighted, emphasizing early recognition and improved clinical outcomes. Full article
(This article belongs to the Special Issue New Discoveries in Calcium Signaling-Related Neurological Disorders)
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18 pages, 1835 KB  
Review
Calcium Signalling in Neurological Disorders, with Insights from Miniature Fluorescence Microscopy
by Dechuan Sun, Mona Amiri, Qi Meng, Ranjith R. Unnithan and Chris French
Cells 2025, 14(1), 4; https://doi.org/10.3390/cells14010004 - 25 Dec 2024
Cited by 10 | Viewed by 2976
Abstract
Neurological disorders (NDs), such as amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and schizophrenia, represent a complex and multifaceted health challenge that affects millions of people around the world. Growing evidence suggests that disrupted neuronal calcium signalling [...] Read more.
Neurological disorders (NDs), such as amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and schizophrenia, represent a complex and multifaceted health challenge that affects millions of people around the world. Growing evidence suggests that disrupted neuronal calcium signalling contributes to the pathophysiology of NDs. Additionally, calcium functions as a ubiquitous second messenger involved in diverse cellular processes, from synaptic activity to intercellular communication, making it a potential therapeutic target. Recently, the development of the miniature fluorescence microscope (miniscope) enabled simultaneous recording of the spatiotemporal calcium activity from large neuronal ensembles in unrestrained animals, providing a novel method for studying NDs. In this review, we discuss the abnormalities observed in calcium signalling and its potential as a therapeutic target for NDs. Additionally, we highlight recent studies that utilise miniscope technology to investigate the alterations in calcium dynamics associated with NDs. Full article
(This article belongs to the Special Issue New Discoveries in Calcium Signaling-Related Neurological Disorders)
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