Sporadic cases of neurodegenerative disease affect millions globally and are characterized by lack of a single known genetic cause. We used Schrödinger’s wavefunction and de Broglie’s wavelength for a non-relativistic particle to model tunneling among principal quantum orbits. Expanding on this work, we described electron behaviour in the brief moment an atom absorbs energy. We then contextualized these findings in a biological setting, positing an imbalance in energy-emitting biochemical reactions lead to structural fluctuations in proteins. Additionally, we prove the cellular microenvironment encourages bonds and behaviour among principal quantum orbits greater than traditionally assumed. Investigating the origin of sporadic disease is crucial for therapies that target the events preceding aggregation.
Sporadic cases of neurodegenerative disease affect millions globally and are characterized by lack of a single known genetic cause. We used Schrödinger’s wavefunction and de Broglie’s wavelength for a non-relativistic particle to model tunneling among principal quantum orbits. Expanding on this work, we described electron behaviour in the brief moment an atom absorbs energy. We then contextualized these findings in a biological setting, positing an imbalance in energy-emitting biochemical reactions lead to structural fluctuations in proteins. Additionally, we prove the cellular microenvironment encourages bonds and behaviour among principal quantum orbits greater than traditionally assumed. Investigating the origin of sporadic disease is crucial for therapies that target the events preceding aggregation.
Findings related to quantum mechanics over the last century have had a pivotal role in our understanding of key physical, chemical, and biological features. Using manipulations of Schrödinger’s wavefunction, we describe electron tunneling through orbits. We extend our findings to a biological setting where we theorize an imbalance in exothermic biochemical reactions may contribute to protein damage. Additionally, we posit the cellular environment encourages electron binding among higher principal quantum orbits than traditionally assumed. This model can be one of many explanations for the sporadic nature of neurodegenerative disease where protein damage, misfolding, or aggregation is a key characteristic.
Findings related to quantum mechanics over the last century have had a pivotal role in our understanding of key physical, chemical, and biological features. Using manipulations of Schrödinger’s wavefunction, we describe electron tunneling through orbits. We extend our findings to a biological setting where we theorize an imbalance in exothermic biochemical reactions may contribute to protein damage. Additionally, we posit the cellular environment encourages electron binding among higher principal quantum orbits than traditionally assumed. This model can be one of many explanations for the sporadic nature of neurodegenerative disease where protein damage, misfolding, or aggregation is a key characteristic.
Abstract This work emphasized the importance of quantum principles in Biological systems. Specially theoretically explained the mechanisms of infectious disease according to the laws of quantum mechanics, focusing on quantum tunneling. It determines the role of quantum events in microbial processes and demonstrates Schrödinger's prophetic view of quantum theory. Interactions between viruses and cells, as well as enzyme function and binding, are not well explained by traditional lock-and-key methods, while quantum tunneling, which is used to pass electrons through this method, can best demonstrate the function of spiked proteins with cellular receptors.
We address into a neuronal system modeled as a two-neuron system, exploring the impact of diverse factors and external perturbations on correlations and information processing capabilities. Incorporating elements such as protein aggregation, synaptic dysfunction, Hopfield coupling, neuronal loss and non-Markovian dephasing noise, the analysis reveals the system’s sensitivity to parameters like synaptic dysfunction, protein aggregation, temperature, coupling strength and non-Markovian factor. Notably, heightened synaptic dysfunction enhances both purity and nonlocality by disrupting local processing and fostering global correlations, while protein aggregation disrupts correlations and increases uncertainty. Hopfield coupling initially enhances correlations but exacerbates uncertainty over time, while neuronal loss and temperature rapidly deteriorate correlations and elevate uncertainty, underscoring the importance of structural integrity in maintaining coherent information processing. This interdisciplinary research advances understanding of neuronal dynamics from a quantum perspective, offering insights into neurodegenerative diseases and paving the way for innovative diagnostic and therapeutic approaches.
Abstract This study introduces a geometric framework to explain how quantum particles, specifically protons, move through energy barriers in biological molecules like DNA. Rather than viewing this tunneling as a purely random event, we propose that it is governed by the structural complexity of the surrounding molecular environment. By treating the energy landscape as a geometric shape, we demonstrate that the environment acts as a regulator that either facilitates or hinders the movement of protons between genetic base pairs. We applied this model to compare the two primary building blocks of the DNA ladder: the Guanine-Cytosine (G-C) and Adenine-Thymine (A-T) pairs. Our findings reveal that the G-C pair possesses a structural configuration that makes proton movement significantly more likely compared to the A-T pair. This difference provides a clear physical explanation for why certain parts of our genetic code are more prone to spontaneous changes, or tautomeric shifts, which can lead to mutations. Furthermore, the research explores how the DNA molecule interacts with its surrounding cellular noise (e.g. water molecules and proteins). We find that the proton behaves in a hybrid manner (at times acting like a coherent wave that exists in multiple places at once), and at other times like a solid particle trapped by its environment. This dual behavior suggests that life operates at a delicate balance between quantum mechanical effects and classical stability.
The spread of the COVID-19 virus has become a global health crisis, and finding effective treatments and preventions is a top priority. The field of quantum biology primarily focuses on energy or charge transfer, with a particular emphasis on photosynthesis. However, there is evidence to suggest that cellular receptors such as olfactory or neural receptors may also use vibration-assisted electron tunnelling to enhance their functions. Quantum tunnelling has also been observed in enzyme activity, which is relevant to the invasion of host cells by the SARS-CoV-2 virus. Additionally, COVID-19 appears to disrupt receptors such as olfactory receptors. These findings suggest that quantum effects could provide new insights into the mechanisms of biological systems and disease, including potential treatments for COVID-19. We have applied the open quantum system approach using Quantum State Diffusion to solve the non-linear stochastic Schrödinger equation (SSE) for COVID-19 virus infection. Our model includes the mechanism when the spike protein of the virus binds with an ACE2 receptor is considered as dimer. These two entities form a system and then coupled with the cell membrane, which is modelled as a set of harmonic oscillators (bath). By simulating the SSE, we find that there is vibration-assisted electron tunnelling happening in certain biological parameters and coupling regimes. Furthermore, our model contributes to the ongoing research to understand the fundamental nature of virus dynamics. It proposes that vibration-assisted electron tunneling could be a molecular phenomenon that augments the lock-and-key process for olfaction. This insight may enhance our understanding of the underlying mechanisms governing virus-receptor interactions and could potentially lead to the development of novel therapeutic strategies.