Update on Inflammation and Degenerative Brain Disease

Excerpt:

While mapping connections of neurons has become the holy grail of current neuroscience, it is clear that communication of neurons with many other types cells is, also, vitally important to every aspect of brain function.

My comment:

Understanding dementia was placed into the context of understanding how virus-driven energy theft alters the de novo creation of olfactory receptor genes and causes the loss of function that is linked to all pathology via chromatin remodeling. The energy-dependent chromatin remodeling is linked from alternative RNA splicing to supercoiled DNA via the innate immune system and nutrient-dependent RNA-mediated amino acid substitutions.

An example of what is known about biologically-based cause and effect was placed into the context of two very different patent applications. One addresses prevention, the other is referred to as Church’s “billion dollar baby.”

For prevention see: Pheromones and the luteinizing hormone for inducing proliferation of neural stem cells and neurogenesis (2011)

For contrast, this is the billion dollar baby: RNA-Guided Human Genome Engineering (2015)

My comment: Nutrient-dependent pheromone-controlled codon optimality links natural selection for food to RNA-mediated cell type differentiation via amino acid substitutions in all cell types of all individuals of all living genera. Transgenerational epigenetic inheritance is the link to energy-dependent ecological adaptations.

Continuing to place the facts about cell type differentiation into the context of cellular intelligence and evolution, which is what Jon Lieff has done for several years, is a misrepresentation of what is known about biologically-based cause and effect. The facts about cell type differentiation place the experience-dependent energy-dependent de novo creation of olfactory receptor genes first.

The creation of new genes is the holy grail of biology. Misrepresentation of virus-driven energy theft, which causes all inflammation and pathology, is the link to replacing the holy grail of biology with the holy grail of neuroscience: mapping connections among neurons. Even when all the connections are mapped, most serious scientists agree that consciousness will not be found among the connections, and that only epigenetic effects on the connections will be linked to degenerative brain disease via chromatin structure and epigenetically-effected supercoiled DNA.

See: From Fertilization to Adult Sexual Behavior

Excerpt (with my emphasis):

Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.

My comment: In the context of  our section on molecular epigenetics and sex differences that must be linked to alternative splicings of otherwise identical genes via chromosomal rearrangements in sex chromosomes, we included that fact that energy-dependent chromatin remodeling was the link from the alternative splicings to cell type differentiation via chromatin structure. Should we have specifically mentioned that what organisms eat determines the structure of chromatin?

What caused the 20 year-long delay between reporting what was known about role of epigenetically-effected chromatin in RNA-mediated cell type differentiation and what is being reported now in the context of mapping connections of neurons, which Jon Lieff refers to as the holy grail of current neuroscience? How did the holy grail of biology become the holy grail of neuroscience with the change from de novo gene creation to mapping the effects of new genes and the effects of gene losses in different cell types?

See:

Many researchers have reported the link from epigenetically-effected chromatin remodeling to gene regulation. Most have reported the link outside the context of energy-dependent chemical ecology and changes that must link angstroms to ecosystems in all living genera. The alternative is to dismiss everything known to physicists, chemists, and molecular biologists who have already done that.

See for example: Structural diversity of supercoiled DNA  Can you dismiss supercoiled DNA?

See also: Excess of Deleterious Mutations around HLA Genes Reveals Evolutionary Cost of Balancing Selection Can you dismiss what is known about the innate immune system and codon optimality?

See also: Direct interrogation of the role of H3K9 in metazoan heterochromatin function Can you dismiss the role of H3K9?

Reported as: Tight DNA packaging protects against ‘jumping genes,’ potential cellular destruction

Excerpt: 

Scientists discovered that the major developmental function of heterochromatin — a form of tight DNA packaging found in chromosomes — is likely the suppression of virus-like DNA elements known as transposons or ‘jumping genes,’ which can otherwise copy and paste themselves throughout the genome, potentially destroying important genes, and causing cancers and other diseases.

What will be the next think that pseudoscientists are forced to dismiss if they continue to try to support their ridiculous theories?

See also: Grand project to unify global efforts to understand the brain

Excerpt:

As brainy gatherings go, it takes some beating. Neuroscientists are meeting in New York today to agree on a global mission to understand the workings of the human brain and how to fix it when something goes wrong.

The lofty aim of the Coordinating Global Brain Projects meeting is to unify worldwide efforts to study the brain, in the same way that international collaborations have spurred on astronomy, physics and genetics.

“Neuroscience is coming of age, and it’s now ready for big science,” says Rafael Yuste at Columbia University in New York, who organised today’s meeting with Cori Bargmann at Rockefeller University, also in New York. “This is the first real meeting with all the players in the same room together,” says Yuste.

I mentioned the award that Cori Bargmann won in the narrative of this poster presentation, which was published to Youtube March 2, 2016.

See:  RNA mediated molecular epigenetics and virus driven entropy

In two weeks, Cori Bargmann will receive an award that links a single neuron to all works on the lifespan and behavior of the nematode, C. elegans. That neuron integrates information from multiple chemical cues including food, oxygen and pheromones. The integration of the cues controls the expression of social behavior in the context of changes in pH. She is scheduled to present: “Genes, neurons, circuits and behavior: an integrated approach in a compact brain.

Perhaps she realizes there is no further need for her integrated approach, since energy-dependent RNA-mediated pheromone-controlled cell type differentiation has been linked from species of microbes to humans. Others do not seem to be aware of that fact.

See the discussion on the Neuroscience FB group

For example: Misha Zilberter is the first author of Dietary energy substrates reverse early neuronal hyperactivity in a mouse model of Alzheimer’s disease (2013). His work can be compared in the context of my model: Nutrient-dependent/pheromone-controlled adaptive evolution: a model and also this 2016 report on A Genetically Encoded Probe for Live-Cell Imaging of H4K20 Monomethylation

Excerpt:

Critical amino acids for the stability and/or folding of the mintbody were revealed.

Reported as: New Probe Detects Histone Modifications in Live Cells

Excerpt:

Using genetic analysis and X-ray crystallography, the new work has also identified amino acids that are critical to the solubility and conformational stability of the H4K20me1-mintbody. Aberrant folding of the antibody fragments in the cellular cytoplasm usually causes solubility problems, but a potential solution has been found. As such, the researchers have overcome challenges to the performance of antibody fragments in live cells due to solubility issues.

For insight on what might prevent discussion of facts about RNA-mediated amino acid substitutions and cell type differentiation in all living genera, see:

Thanks to Anna Di Cosmo for calling attention to this. (Although he uses foul language to make his point, it is a point that needs to be made.)
 
Unfortunately, using Bill Nye to represent scientists may cause serious scientists to laugh along with anyone among the lay audience who does not believe what people like Bill Nye claim about evolution.
 
Like serious scientists, they may be waiting for Nye to present experimental evidence that links energy-dependent changes from angstroms to ecosystems in all living genera. Only then are they likely to believe that hydrogen-atom transfer in DNA base pairs in solution is contributing to the loss of species via climate warning.
If changes in the pH of the ocean are not considered, what experimental evidence that links ecological variation to ecological adaptation will be considered by those who think the “Science Guy” is biologically uninformed? Why, from his perspective on evolution, aren’t species simply acquiring more beneficial mutations to evolve —  if that’s what theorists want you to believe in?

See also this discussion of As simple as random can be

See also this discussion of  Four things you should know about brain research

What can anyone expect to come from any Grand project to unify global efforts to understand the brain.  All past grand projects have failed to link what is known about biophysically constrained RNA-mediated protein folding chemistry to cell type differentiation in all living genera via what is known about chromatin, which links energy-dependent changes in the microRNA/messenger RNA balance to biophysically constrained cell type differentiation in all living genera, including those with the primitive brain of a nematode or the brain of a conscious human.

Most the grand projects seem designed to support the ridiculous theories of the project organizers.

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