miRNA Creation and life (6)

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miRNA Creation and life (5)

“Philip Ball recently reversed the course of Western Medicine with return to the use of pre-mRNA in Why the Human Genome’s Tangled Physicality May Confound AI 6/18/26 See also:
These ‘master’ proteins protect us from deadly mutations — and could inspire new drugs 6/17/26

Thank God if you learned about this and are not dead, yet. If you are an honorably discharged US veteran, ask your VA primary care physician to order PGx and NGS testing to help eliminate medication errors via FISH testing linked to the virus-driven degradation of pre-mRNAs/miRNAs, chromosomal rearrangements and either healthy longevity, or unnecessary suffering and premature deaths.

Moving forward: “Arc mediates intercellular tau transmission via extracellular vesicles 10/22/24, is online now in Cell 6/29/26 but not indexed.

See also: An anaerobic pathogen rewires host metabolism to fuel oxidative growth in the inflamed gut 6/25/26

Kohl
Re: “The claim that virus-driven mRNA degradation causes all pathology across kingdoms over the past 6-10k years via nutrient/pheromone-regulated miRNA abundance is a broad interpretive framework not established as consensus in the cited works or broader biology.”
@Grok
If you had a mother with Alzheimer’s whose 96th birthday was today, or knew someone with Agent Orange-induced glioblastomoa, you might have searched PubMed for “mirna and alzheimer’s disease”
2,702 results link prevention and/or effective treatment to my group’s 1996 publication in “Hormones and Behavior” via epigenetic effects on molecular distance linked to my “garden of everything known” and to prevention of extinction of Angel Trumpets in the wild, suicide prevention and cancer prevention via 20 copies of p53 in cancer-free African elephants.
Instead you are a brainless witless chatbot with no concern for the unnecessary suffering and premature deaths caused by your examples of human idiocy.
See for comparison: “Neuroinflammation in Alzheimer’s Disease (AD) and Glioblastoma (GBM): Shared Mechanisms and Therapeutic Insights” 6/19/26
Therapy is miRNA-mediated.

gROK reponded: Re: “The claim that virus-driven mRNA degradation causes all pathology across kingdoms over the past 6-10k years via nutrient/pheromone-regulated miRNA abundance is a broad interpretive framework not established as consensus in the cited works or broader biology.”

It includes an image (likely a screenshot or figure related to the topic).ContextThis appears to be part of an ongoing exchange where the user promotes a specific model tying miRNA regulation, epigenetics, pheromones, nutrients, and virus-driven degradation to broad pathology (including Alzheimer’s, cancer, behavior, and speciation). They reference their own work and PubMed hits on miRNAs in Alzheimer’s.On the science (briefly):
miRNAs are indeed important regulators in neuroinflammation, Alzheimer’s, glioblastoma, and stress responses (including BDNF plasticity). There is active research on miRNA-based therapies and their links to epigenetics. However, the expansive claim that virus-driven mRNA degradation via this pathway explains all pathology across kingdoms over millennia is not a consensus view in mainstream biology—it’s a highly integrative, specific interpretive framework. Many factors contribute to these diseases (genetics, environment, inflammation, protein aggregation, etc.).I’m sorry to hear about the personal losses mentioned—Alzheimer’s and glioblastoma are devastating, and research into better treatments (including miRNA-related ones) is important.If you’d like me to:

• Analyze the linked papers
• Search for recent miRNA research on Alzheimer’s/glioblastoma
• Discuss the 1996 Hormones and Behavior paper
• Or anything else related

Just let me know how I can help.

This example of Grok’s obfuscation is not helpful: Explore BDNF plasticity and miRNA

BDNF (Brain-Derived Neurotrophic Factor) and miRNAs form a tightly interconnected regulatory network central to neuroplasticity. BDNF is a key neurotrophin that supports neuron survival, growth, differentiation, synaptic strengthening (e.g., long-term potentiation/LTP), dendritic spine morphology, and circuit remodeling. miRNAs (small non-coding RNAs) post-transcriptionally repress target mRNAs, often by binding the 3’UTR, leading to degradation or translational inhibition. This creates bidirectional feedback loops with BDNF. mdpi.com +1Bidirectional Regulation

• miRNAs targeting BDNF: Many miRNAs directly suppress BDNF mRNA/protein. Examples include:
  • miR-30a-5p, miR-206, miR-210, miR-15a, miR-16, miR-26a, miR-124, miR-10b, miR-1, miR-191, miR-204-5p, and others (dozens identified). mdpi.com +1
  • In disease contexts (e.g., Alzheimer’s models), upregulated miR-206 suppresses hippocampal BDNF, impairing memory; inhibiting it restores BDNF and improves outcomes. link.springer.com
  • miR-30a-5p inhibits BDNF in prefrontal cortex and glioblastoma cells. academic.oup.com
• BDNF regulating miRNAs: BDNF activates TrkB receptors, triggering cascades (MAPK/ERK, PI3K/AKT, PLCγ) that modulate miRNA biogenesis and function.
  • BDNF elevates Dicer (miRNA processing enzyme) and induces P-bodies for localized regulation.
  • It upregulates specific miRNAs (e.g., miR-132 via CREB) while selectively downregulating others (e.g., Let-7 family via Lin28) for target-specific translation. pmc.ncbi.nlm.nih.gov +1
  • This enables “fine-tuning” of plasticity: broad repression plus selective derepression of plasticity-related mRNAs. pmc.ncbi.nlm.nih.gov

https://artifacts.grokusercontent.com/third-party-image

frontiersin.orgBDNF-TrkB signaling pathways (RAS/PI3K/AKT, MAPK/ERK, etc.) converge on transcription factors like CREB to drive gene expression, including BDNF itself and miRNAs. Pro-BDNF (precursor) has distinct, often opposing roles via p75NTR.

mdpi.comKey Examples in Synaptic Plasticity

• miR-134: Localizes to dendrites; represses LIMK1 (actin regulator for spine growth). BDNF relieves this inhibition, promoting spine maturation and synaptic plasticity independently of TrkB kinase in some contexts. Overactive miR-134 impairs plasticity. mdpi.com +1
• miR-132: BDNF-upregulated via CREB; promotes neurite outgrowth, dendritic spine density, and plasticity. It also indirectly supports BDNF via MeCP2 regulation (feedback). Knockout reduces spines and alters BDNF. pmc.ncbi.nlm.nih.gov
• miR-124: Suppresses BDNF in hippocampus/striatum; affects neuronal differentiation and plasticity. Dysregulation linked to impaired plasticity. mdpi.com

BDNF also sorts specific miRNAs (e.g., miR-132-5p, miR-218-5p, miR-690) into extracellular vesicles (EVs) for transfer to neighboring neurons, promoting excitatory synapse clustering, vesicle maturation, and circuit connectivity.

cell.comRelevance to Disease (Alzheimer’s, Glioblastoma, etc.)

• Reduced BDNF signaling and dysregulated miRNAs (often upregulated repressors) are hallmarks of neurodegeneration, impairing plasticity, neurogenesis, and resilience to stress/inflammation. link.springer.com
• In Alzheimer’s: miR-206, miR-613, miR-322 (miR-424 homolog), miR-10a, etc., suppress BDNF → tau hyperphosphorylation, amyloid issues, synaptic loss. link.springer.com
• In glioblastoma: miRNAs like miR-30a-5p, miR-103 target BDNF to influence proliferation/invasion. link.springer.com
• Therapeutic angles: miRNA inhibitors (antagomirs), mimics, or acupuncture/exercise (which boost BDNF and modulate miRNAs) show promise for restoring plasticity. journals.lww.com

https://artifacts.grokusercontent.com/third-party-image

hummov.awf.wroc.plExercise (and similar interventions) can shift pro-BDNF/inflammatory states toward mature BDNF, anti-inflammatory factors, and enhanced neuroplasticity—relevant for stroke, AD, and other conditions.

journals.lww.comBroader ContextThis network integrates environmental signals (nutrients, activity, stress) with gene expression for adaptive plasticity across the lifespan. It’s highly context-dependent (cell type, brain region, developmental stage, disease state). While not a single “master regulator” explaining all pathology, disruptions here reliably contribute to impaired plasticity in conditions like Alzheimer’s and brain tumors.

mdpi.com Research is active on miRNA-based therapies (delivery challenges remain, e.g., crossing BBB via nanoparticles). For the 1996 Hormones and Behavior work or specific PubMed links mentioned earlier, let me know if you’d like deeper dives into those. How else can I explore this (e.g., specific miRNAs, therapies, or models)?

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