Abstract

This paper introduces a computational model that underlies an electromagnetic theory of inter-neuronal interactions in the human brain. This hypothesis behind this model aims to explain human perception, cognition, memory and consciousness and involves an interdisciplinary approach combining biophysics, holography, and neuroscience. The main assumption used is that the phospholipid head groups of neuronal membranes, when stimulated energetically by the electric fields of propagating action potentials, can generate a metastable coherent state giving rise to an electromagnetic field. This is consistent with the Froehlich theory of biological coherence. Additionally, the electromagnetic fields produced by neighboring neurons can create interference patterns that lead to the formation of holographic images. This mechanism can solve the binding problem of consciousness where external sensory inputs are transduced into conscious perceptions. 

Keyword: Bioinformatics, brain complexity, neurodegeneration, integrative multi-omics approaches, neurodevelopmental 

How to Cite this Article: Marco Cavaglia and Jack Tuszynski (2025). A physical model of neuronal membrane excitations as a mechanism of holographic image formation in brain. Journal of Multiscale Neuroscience, 4(3):187-195 DOI: https://doi.org/10.56280/1704135468 

Authors Affiliation: 

• Marco Cavaglia DIMEAS, Politecnico di Torino, Corso Duca degli Abruzzi 24, Torino I-10129, Italy 

• Jack Tuszynski DIMEAS, Politecnico di Torino, Corso Duca degli Abruzzi 24, Torino I-10129, Italy 

Conflict of Interest: The authors declare no conflict of interest 

Copyright: © 2025 The Author(s). Published by Neural Press. This is an open access article distributed under the terms and conditions of the CC BY-NC-ND 4.0 license. 

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, Neural Press or the editors, and the reviewers. Any product that may be evaluated in this article, or claim that made by its manufacturer, is not guaranteed or endorsed by the publisher.

Abstract

Autism spectrum disorder does not include anxiety as one of its core features, which has its own unique and additional level of complexity. The prevalence of anxiety disorder is not considered a core dimension, yet majority of individuals with autism exhibit clinically elevated levels of anxiety or suffer from at least one anxiety disorder, including obsessive-compulsive disorder. Individuals with anxiety are more susceptible to heightened and prolonged negative emotional states, which are indicative of potential dysfunctions within the brain systems responsible for regulating negative emotions. Anxiety is believed to have a neurobiological component, and considerable research has long been conducted to determine how its arousal impacts behavioral development in typical situations. Investigation has focused on the structural development of the amygdala implicated in the neurobiology of autism. An overview of the role of the prefrontal cortex in modulation of amygdala function is presented in this paper, as well how differences in amygdala and prefrontal cortex connectivity may play a role in influencing the presentation of anxiety syndrome in the context of autism spectrum disorder. 

Keywords: Autism Spectrum Disorder (ASD), anxiety, amygdala, neural circuits, brain connectivity, functional connectivity, neural mechanisms, emotion regulation, anxiety pathways in autism 

How to cite this paper Lleuvelyn A. Cacha, Dolores Mirabueno and Lourdes P. Terrado (2025) The Neurobiology of Fear: Understanding Anxiety in Autism Spectrum Disorder. Journal of Multiscale Neuroscience 4(3), 196-207. DOI: https://doi.org/10.56280/1713559115 

Author Affiliation: 

• Lleuvelyn A. Cacha, Graduate School Research Coordination University of the East, Manila. 

• Dolores Mirabueno, College of St Benilde, De La Salle University.

• Lourdes P. Terrado Graduate School University of the East, Manila. 

Conflict of Interest: The author declares no conflict of interest Copyright: © 2025 The Author(s). Published by Neural Press. This is an open access article distributed under the terms and conditions of the CC BY-NC-ND 4.0 license. 

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, Neural Press or the editors, and the reviewers. Any product that may be evaluated in this article, or claim that made by its manufacturer, is not guaranteed or endorsed by the publisher.

Abstract

Since the onset of intracellular voltage recording techniques, additional methods have been developed and improved upon, such as using voltage-activated dyes, sodium indicators, fluorescent proteins (namely Green fluorescent protein (GFP)), synthetic and genetically encoded indicators, in conjunction with calcium imaging Gasparini & Palmer (2016). These techniques have shown that dendrites are not just simple transmission lines, but are sophisticated cellular systems with nonlinear multiscale dynamics that evolve over different timescales and are involved in neural signaling, information processing, along with any underlying computations. Calcium imaging has been important in this regard, having highlighted how reaction-diffusion processes between calcium, buffers and other proteins shape neuronal activity, through dynamical interaction and synaptic plasticity, over different timescales compared to the evolution of electrical signals. To this end, experiments have shown the involvement of calcium and calcium dependent buffers in the response dynamics of neurons. A novel participant during morphological studies, using electron microscopy, fluorescence and immunostaining have illustrated that the Endoplasmic Reticulum (ER) (present in the soma and extends into the distal dendrites) is also a calcium store that can release calcium as puffs through the activation ryanodine receptors into the cytosol of neuronal dendrites. This is called Ca2+ -induced Ca2+ release (CICR), which have been implicated in a number of processes, including the occurrence of calcium waves in the presence of a unsaturated buffer. In this situation, one can observe local changes to the Ca2+ and buffer concentrations in response to some stimuli, such as the presentation of orientated stationary or moving bars or gratings, in a selective fashion through the manifestation of a bias in the resulting calcium concentration in space along the dendrite, that underpins some computation. Studies have shown that Ca2+ plays many important roles in neuronal function and information processing. To better understand the role of Ca2+, we constructed a computational model of a dendrite with a mechanism that describes CICR in the presence of an unsaturated buffer and study the conditions permitting the occurrence calcium waves and the underlying requirements of timed inputs from CICR. Modeling the heterogeneity of CICR from the endoplasmic reticulum by using a formulation that permits essential dynamics to be analyzed. Using a two-pool model calcium dynamics, we present an analysis of how CICR impacts calcium activity in space in the presence of a calcium buffer and study the potential conditions supporting the propagation of CICR induced Ca2+ waves. 

Keywords: Endoplasmic reticulum, Calcium ions, Calcium-Induced-Calcium Release mechanism, Two-pool calcium model. 

Cite this paper as: Iannella N & Poznanski R (2025). Spatiotemporal Ca dynamics in neuronal dendrites: Responses and support of travelling waves. Journal of Multiscale Neuroscience 4(3): 208-220 DOI: https://doi.org/10.56280/1714100811 

Author Affiliation: 

• Nicolangelo Iannella, Department of Biosciences, University of Oslo, Norway 

• Roman Poznanski, Bion Institute, SI-1000 Slovenia, EU. 

Conflict of Interest: The author declares no conflict of interest 

Copyright: © 2025 The Author(s). Published by Neural Press. This is an open access article distributed under the terms and conditions of the CC BY-NC-ND 4.0 license. 

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, Neural Pres or the editors, and the reviewers. Any product that may be evaluated in this article, or claim that made by its manufacturer, is not guaranteed or endorsed by the publisher

Abstract

Consciousness arises from physical and geometric constraints, yet the nature of phenomenality remains unresolved. A conceptual and mechanistic framework links self-intending projection to phenomenal consciousness. Based on Dynamic Organicity Theory, this materialist framework posits that quantum effects underlie phenomenality. Moving beyond representational models, Embedded Quantum Physicalism (EQP) offers a multiscale, non-reductive approach in which consciousness is naturalized through effective processes embedded within the brain’s functional geometry. This geometry evolves through functional interactions that constrain internal states, while its curvature organizes agential holons and intrinsic information into self-referential loops, enabling intentional closure via self-intending projections. Reflexivity alone is insufficient; intrinsic intentionality emerges from these loops and provides the necessary condition for consciousness. Under EQP, phenomenality is not an ontological primitive but a physically instantiated phenomenon. Unlike reductive accounts that reduce consciousness to neural correlates or dismiss it as epiphenomenal, EQP traces phenomenality to thermo-quantum fluctuations in the brain’s biochemistry, which reshape functional geometry. This geometry supports effective processes, including projections, holonomies, and projective closure. Toroidal-like neuropil microcavities enter coherent quasipolaritonic modes through quantum-optical effects, involving delocalized information systems that transform intrinsic information. Phenomenality arises when stable agential holons form self-intending projections with projective closure, embodied in a Weyl-like, non-Euclidean functional geometry shaped by effective quantum potentials acting as lensing mechanisms at small scales in the neuropil. 

Keywords: Phenomenality, nonreductive physicalism, effective theory, quasi-strong emergence, functional holonomy, projection, quantum potential geometry, self-referential intentionality, post-structural dynamics, microcavities, process realism. 

How to cite this paper: Roman R. Poznanski (2025) Unfolding functional brain geometry across scales: self-intending projection framework for phenomenal consciousness. Journal of Multiscale Neuroscience, 4(3); 221-243. DOI: https://doi.org/10.56280/1714720458 

Author Affiliation: Roman R Poznanski, BION Institute, Slovenia.

Conflict of Interest: The author declares no conflict of interest 

Copyright: © 2025 The Author(s). Published by Neural Press. This is an open access article distributed under the terms and conditions of the CC BY 4.0 license. 

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, Neural Press or the editors, and the reviewers. Any product that may be evaluated in this article, or claim that made by its manufacturer, is not guaranteed or endorsed by the publisher

Abstract

Alzheimer’s disease (AD) is characterized by amyloid-β accumulation and tau hyperphosphorylation, leading to neurodegeneration and cognitive decline. Photobiomodulation (PBM) has shown promise in mitigating AD pathology, yet its effects on tau remain poorly understood. We investigated the impact of high-polarized light (HPL; Bioptron Quantum Hyperlight, 350–3400 nm) on tau phosphorylation using an ex vivo rat brain slice model of synthetic torpor (ST), a reversible hypometabolic state inducing controlled tau hyperphosphorylation. Slices were incubated at physiological (37 °C) or hypometabolic (25 °C) temperatures and exposed to HPL for 10 or 20 minutes. Western blot analyses of Tau-1 (non-phosphorylated tau), p-GSK3β (Ser9), and p-T205 revealed that HPL increased Tau-1 levels in warm slices, indicating a shift toward reduced tau hyperphosphorylation. p-GSK3β modulation was variable, reflecting inter-animal differences and temperature-dependent kinase/phosphatase dynamics. Cold slices exhibited smaller, more heterogeneous responses, consistent with suppressed metabolic activity and attenuated PBM signaling. Site-specific p-T205 changes suggest transient kinase activation and redox signaling, compatible with an overall trend toward normalized tau phosphorylation. These results highlight how HPL can modulate tau phosphorylation ex vivo, with the most consistent effects under normothermic conditions. Despite limitations, our findings provide preliminary evidence supporting HPL/PBM as a potential therapeutic strategy for tauopathies. Future in vivo studies are warranted to elucidate mechanisms, optimize dosing, and explore glymphatic-mediated clearance in PBM-treated brains. 

Keywords: photobiomodulation, hyperpolarized light, Alzheimer, hypothermia, synthetic torpor, tau hyperphosphorylation 

How to Cite this paper: Emiliana Piscitiello, Barbara Truglia, Sara Castria, Alessandra Occhinegro, Elisa De Angelis, Luca Alberti, Ludovico Taddei, Timna Hitrec, Roberto Amici, Jack A. Tuszynski, Marco Luppi (2025) Ex vivo modulation of tau phosphorylation by hyperpolarized light: implications for Alzheimer’s disease therapy, Journal of Multiscale Neuroscience 4(3), 244-256. DOI: https://doi.org/10.56280/1714956796 

Author Affiliation: 

• Emiliana Piscitiello, University of Bologna, Department of Biomedical and Neuromotor Sciences, Bologna, Italy, 40127. 

• Barbara Truglia, University of Alberta, Faculty of Engineering, Department of Biomedical Engineering, Edmonton, Canada, T6G1H9. 

• Sara Castria, Politecnico di Torino, Faculty of Engineering, Department of Mechanical and Aerospace Engineering (DIMEAS), Turin, Italy, 10129. 

• Alessandra Occhinegro, University of Bologna, Department of Biomedical and Neuromotor Sciences, Bologna, Italy, 40127. 

• Elisa De Angelis, University of Bologna, Department of Biomedical and Neuromotor Sciences, Bologna, Italy, 40127. 

• Luca Alberti, University of Bologna, Department of Biomedical and Neuromotor Sciences, Bologna, Italy, 40127. 

• Ludovico Taddei, University of Bologna, Department of Biomedical and Neuromotor Sciences, Bologna, Italy, 40127. 

• Timna Hitrec, University of Bologna, Department of Biomedical and Neuromotor Sciences, Bologna, Italy, 40127. 

• Roberto Amici, University of Bologna, Department of Biomedical and Neuromotor Sciences, Bologna, Italy, 40127. 

• Jack A. Tuszynski, University of Alberta, Faculty of Science, Department of Physics, Edmonton, Canada, T6G2E1. Politecnico di Torino, Faculty of Engineering, Department of Mechanical and Aerospace Engineering (DIMEAS), Turin, Italy, 10129. 

• Marco Luppi, University of Bologna, Department of Biomedical and Neuromotor Sciences, Bologna, Italy, 40127. 

Conflict of Interest: The author declares no conflict of interest 

Copyright: © 2025 The Author(s). Published by Neural Press. This is an open access article distributed under the terms and conditions of the CC BY-NC-ND 4.0 license. 

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, Neural Press or the editors, and the reviewers. Any product that may be evaluated in this article, or claim that made by its manufacturer, is not guaranteed or endorsed by the publisher