I have proposed leronlimab as treatment for neurod
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Posted On: 06/22/2023 9:16:00 PM
I have proposed leronlimab as treatment for neurodegenerative diseases based on leronlimab fixing secondary causes.
A new study out leads me to believe that leronlimab goes straight to the core of the matter and can stop many neurodegenerative diseases right from the start. The study shows that abnormal length glutamines called polyglutamines start the entire chain reaction of amyloid deposition.
CCR5 via CCL3, CCL4, and CCL5 (RANTES) sharply decrease the cell death (autophagy) that would eliminate these abnormal polyglutamines. Leronlimab of course would reverse this and could stop polyglutamine based neuronal disorders from occurring.
Very likely that many other neurodegenerative disorders not associated with polyglutamines follow a similar path but with other abnormal proteins. So leronlimab would most likely be helpful in those diseases also. This is the kind of thing that gets me excited.
A new study out leads me to believe that leronlimab goes straight to the core of the matter and can stop many neurodegenerative diseases right from the start. The study shows that abnormal length glutamines called polyglutamines start the entire chain reaction of amyloid deposition.
Quote:
New research reveals the start of Huntington’s disease
https://www.stowers.org/news/new-research-fro...ns-disease
Quote:
Pathologic polyglutamine aggregation begins with a self-poisoning polymer crystal
https://elifesciences.org/reviewed-preprints/86939
CCR5 via CCL3, CCL4, and CCL5 (RANTES) sharply decrease the cell death (autophagy) that would eliminate these abnormal polyglutamines. Leronlimab of course would reverse this and could stop polyglutamine based neuronal disorders from occurring.
Quote:
Microglial-to-neuronal CCR5 signaling regulates
autophagy in neurodegeneration
https://www.cell.com/neuron/pdf/S0896-6273(23)00268-4.pdf
Quote:
Aggregate-prone proteins with polyglutamine and polyalanine expansions are degraded by autophagy
[url=Aggregate-prone proteins with polyglutamine and polyalanine expansions are degraded by autophagy]Aggregate-prone proteins with polyglutamine and polyalanine expansions are degraded by autophagy[/url]
Very likely that many other neurodegenerative disorders not associated with polyglutamines follow a similar path but with other abnormal proteins. So leronlimab would most likely be helpful in those diseases also. This is the kind of thing that gets me excited.
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