The diet-driven construction of the competing endogenous RNA networks (ceRNA networks) is energy-dependent and biophysically constrained by the pheromone-controlled physiology of reproduction. Viruses compete for the energy, which is how they contribute to the degradation of messenger RNA that all serious scientists have linked to all mental and physical pathology.

Cell death is not just seen in the context of autophagy and neural cell death. The pathogens that alter physiology also alter behavior via the conserved molecular mechanisms of energy-dependent RNA interference.

See for instance: Molecular Network-Based Identification of Competing Endogenous RNAs in Thyroid Carcinoma

In the future, more attention should be paid to the construction of ceRNA networks and the validation of biomarkers or RNA competing endogenous interactions.

MicroRNAs are the biomarkers that link diet-driven RNA competing endogenous interactions from RNA interference to mental health or to mental disorders.

See for comparison:  Interactions between neurotropic pathogens, neuroinflammatory pathways, and autophagic neural cell death

The presence of antigenic stimuli of pathogens can induce autophagic genes through a stratified array of principal immunologic processes, and therefore result in augmented autophagy and inflammation at the site of infection, which is considered to be protective to the host. However, an excessive auto-degeneration of the neuronal cells can be harmful. The question arises, whether there are any known direct interactions of intracellular pathogens (having neurotropism) with this degradative pathway that favor the pathogens for intracerebral survival and growth? It is worth exploring if there is any cooperation between pathogen factors altering immune inflammatory pathways, thereby influencing host cell autophagy regulatory genes that cause massive neuronal damage in intracranial infections as hypothesized presently [Figure 1]. Targeting some key pathways with respect to infectious causes of neurodegeneration will be the need of tomorrow’s new drug discovery that may or may not include the targeting of autophagy for minimizing brain matter degeneration.

There are many ways to say the same thing, and that is what’s happening in the context of their claims about  autophagic neural cell death.

See: Reduced expression of brain-enriched microRNAs in glioblastomas permits targeted regulation of a cell death gene

The virus-driven degradation of messenger RNA is the link to neurodegeneration and to the activation of death genes in all cell types of all tissues of all individuals of all living genera.

The interactions among pathogens, inflammatory pathways, and autophagy can be viewed from the bottom-up. See: Virus-mediated archaeal hecatomb in the deep seafloor

We show here for the first time the crucial role of viruses in controlling archaeal dynamics and therefore the functioning of deep-sea ecosystems, and suggest that virus-archaea interactions play a central role in global biogeochemical cycles.

The interactions among pathogens, inflammatory pathways, and autophagy can be viewed from the top-down.

Analysis of experience-regulated transcriptome and imprintome during critical periods of mouse visual system development reveals spatiotemporal dynamics

Visual system development is light-experience dependent, which strongly implicates epigenetic mechanisms in light-regulated maturation. Among many epigenetic processes, genomic imprinting is an epigenetic mechanism through which monoallelic gene expression occurs in a parent-of-origin-specific manner.

Monoallelic gene expression in olfactory neurons links parent-of-origin-specific epigenetic effects on genetic predispositions to all cell type differentiation via transgenerational epigenetic inheritance of morphological and behavioral phenotypes.  

See for comparison: Evolution unleashed: Is evolutionary science due for a major overhaul – or is talk of ‘revolution’ misguided? 

If evolution is not to be explained solely in terms of changes in gene frequencies; if previously rejected mechanisms such as the inheritance of acquired characteristics turn out to be important after all; and if organisms are acknowledged to bias evolution through development, learning and other forms of plasticity – does all this mean a radically different and profoundly richer account of evolution is emerging? No one knows:…

The late-breaking claim that “No one knows” can be compared to what is known to all serious scientists about molecular epigenetics. See for an unchanged historical perspective: From Fertilization to Adult Sexual Behavior

See also:  Epigenetic mechanisms underlying nervous system diseases 

 

Re: “…evolving profiles of cell-extrinsic, cell-cell, and cell-intrinsic signals. These dynamic processes are responsible for mediating cell- and tissue-specific gene expression and function…”

The biophysically constrained profiles do not evolve. They link ecological variation to ecological adaptation via RNA-mediated protein folding chemistry. The protein folding chemistry links energy-dependent changes in base pairs to fixation of amino acid substitutions in the cell types of all individuals of all species.

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