LOS ANGELES — At this year’s largest conference on Alzheimer’s disease, there was no big reveal. There were no major companies presenting late-stage data on promising therapies. There was little in the way of groundbreaking research.
Instead, there was a sense from many researchers in the field that, after a string of high-profile clinical trial failures, there is nowhere to go but back to the drawing board.
“The field is confused, disoriented, and completely devastated. We don’t have a lot of positive news these days,” said Martin Tolar, CEO of Alzheon, one of the few companies left standing in the Alzheimer’s space. “But I do believe there’s a lot of incredible science built over the past 20 years.”
I am astonished that nothing was mentioned about the new biomarker found by German researchers to potentially predict Alzheimer/dementia much earlier as tweeted by Bill Gates (he has over $40m dedicated to different funds and foundations for this research).
Also, Neuroinflammation is now recognized of the true cause to the serious degenerative diseases such as Parkinson, Alzheimer and Dementia. LPS ( metabolites toxic to Neurons and blood vessel cells like heart cells) are causing inflammatory reactions. LPS and bad bacteria can pass the gut lining. The Gut microbiome – Brain connection is well described.
Light-activated microRNA biogenesis in plants links the energy as information-dependent assembly of the microRNA-RNA-peptide nanocomplex to biophysically constrained viral latency.
Viral replication causes the creation of toxic peptides that link mutations to all pathology. For contrast, food energy-dependent pheromone-controlled microRNA-mediated fixation of RNA-mediated amino acid substitutions has been linked to healthy longevity in species from human gut microbes to humans.
After the facts were placed into the context of the EDAR V370A allele in human populations in the Old World and the New World, researchers from Iran asked: “Why have microRNA biomarkers not been translated from bench to clinic?”
Researchers from South Korea hinted at the answer. It’s likely to be that linking the sun’s anti-entropic virucidal energy to biophysically constrained viral latency or linking viral replication to all pathology refutes neo-Darwinian pseudoscientific nonsense and every aspect of Big Bang cosmology.
Who is going to fund research that refutes all the ridiculous theories, despite more than 89,000 published works that mention microRNAs, which are indexed on PubMed?
There is exciting new evidence for the potential of Galectin-3 as a therapeutic target for Alzheimer’s Disease.
Galectin Therapeutics has a Galectin-3 inhibitor in clinical trials for NASH fibrosis and cancer immunotherapy combinations with aPD-1.
Since the Galectin-3 pathway is implicated in a number of inflammatory and fibrotic diseases, it is not too surprising that it might play a role in AD.
Here are some papers with eye-opening findings:
1. Galectin 3, a novel endogenous TREM2 ligand, detrimentally regulates inflammatory response in Alzheimer’s disease
“In this work, we demonstrate (1) a significant upregulation of gal3 in human AD patients compared to age-matched healthy controls, (2) the preferential expression of gal3 in microglial cells in contact with Aβ plaques both in human and mouse, (3) a clear reduction of the inflammatory response in microglial cells challenged with Aβ fibrils (fAβ) following gal3 inhibition and gal3 deletion in microglial cultures, (4) a significant Aβ plaque reduction and better cognitive outcome in 5xFAD mice lacking gal3, and (5) the role of gal3 as a ligand of TREM2 through its carbohydrate recognition domain (CRD) domain, which confers the ability to bind glycans.”
“Overall, our data support the view that gal3 inhibition may be a potential pharmacological approach to counteract AD.”
2. Galectin-3 promotes Aβ oligomerization and Aβ toxicity in a mouse model of Alzheimer’s disease
“Because Gal-3 expression is dramatically increased as early as 3 months of age in APP/PS1 mice and anti-Aβ oligomerization is believed to protect against Aβ toxicity, Gal-3 could be considered a novel therapeutic target in efforts to combat AD.”
3. Galectin-3 Inhibition Is Associated with Neuropathic Pain Attenuation after Peripheral Nerve Injury
“Intrathecal administration of modified citrus pectin (MCP), a gal3 inhibitor, reduces gal3 expression in dorsal root ganglions. MCP treatment also inhibits SNL-induced gal3 expression in primary rat microglia.” (note: GR-MD-02 is similar to MCP)
4. Galectin-3 initiates epithelial-stromal paracrine signaling to shape the proteolytic microenvironment during corneal repair
“We show that single fibroblasts activated the MMP-9 promoter in clustered epithelial cells after the induction of direct heterotypic cell-cell contacts. We further demonstrated that this effect was mediated by galectin-3 of epithelial origin and involved the activation of a fibroblast-dependent paracrine mechanism of IL-1β secretion.”
5. Matrix Metalloproteinases and Their Multiple Roles in Alzheimer’s Disease
“Serum levels of MMP-9 were also found elevated in AD compared to controls and patients suffering from mild cognitive impairment. Under these conditions, the increase in MMP-9 expression tends to be characteristic of AD.”
Now we would just need patient advocacy groups to help raise awareness of this possibility and maybe this might lead to starting a clinical trial for this indication with GR-MD-02.
“Pheromones and the luteinizing hormone for inducing proliferation of neural stem cells and neurogenesis” links what is know about food energy-dependent biophysically constrained viral latency (RNA interference) from the mouse-to-human model via “Pheromonal regulation of genetic processes: research on the house mouse (Mus musculus L.)”
I am relieved, , hopeful and delighted that this new investigated approach to this illness will be commencing.
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