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New drug never been posted hooray
im russian so dont expect everything to be grammatically correct negroids
Also always DO YOUR OWN RESEARCH
im russian so dont expect everything to be grammatically correct negroids
Also always DO YOUR OWN RESEARCH
J147, derived from curcumin with structural modifications for enhanced central nervous system bioavailability and mitochondrial affinity, interacts primarily with mitochondrial ATP synthase, particularly targeting daATP5A subunit. This interaction moderates mitochondrial membrane potential and cellular ATP levels, important for neuronal metabolic stability and helps against excitotoxic stress
By diminishing ATP synthase activity, regulates mitochondrial membrane potential, important in maintaining neuronal metabolic stability. This helps protect cells under bioenergetic stress by maintaining ATP levels through alternative metabolic pathways, increased glycolytic flux, important in neurons where ion homeostasis deregulation contributes to Alzheimers pathogenesis
It enhances neuroprotective pathways and neuroplasticity through upregulation of brain derived neurotrophic factor (BDNF). This involves secondary signaling cascades activated via mitochondrial biogenesis promoters and sirtuin pathways, especially SIRT1, cuz its affects in neural longevity and stress resistance. Enhanced BDNF expression promotes synaptic plasticity and resilience, helping memory and learning
It affects amyloid precursor protein (APP) processing, reducing amyloidogenic cleavage of APP which results in accumulation of beta amyloid plaques, a mark of Alzheimer's pathology. This modification is partly achieved by changing activity of secretase enzymes, primarily beta secretase 1 (BACE1), potentially via changes in enzyme expression or cellular localization
It has an anti-inflammatory effect within the central nervous system by modulating microglial activity, the brain's immune cells. This is achieved by downregulating pro-inflammatory cytokines and upregulating anti-inflammatory cytokines, mediated through NF-kB signaling pathways. Changing microglial activation reduces the neuroinflammatory response, important in slowing neurodegeneration in Alzheimers
Its lipophilicity and molecular weight are optimized for penetration across the blood brain barrier, issue for many neurotherapeutic agents. Once in the brain, It accumulates in regions like the hippocampus and cerebral cortex, related to Alzheimer’s pathology, where it executes its neuroprotective actions
- Animal Models: Doses in rats are from 1 to 30 mg/kg, orally
- Human dose based on animal studies, uses a conversion method based on body surface area. Animal data suggests a range of 1 to 30 mg/kg for rodents:
- Human dose based on animal studies, uses a conversion method based on body surface area. Animal data suggests a range of 1 to 30 mg/kg for rodents:
FDA gives a conversion factor to convert animal doses to human doses based on body surface area. It's 12.3 for rodents.
- Dosing Range: If converting these from animal models to human use, you could consider a starting dose somewhere within this range, 0.08mg/kg - 2.44mg/kg
- Dosing Schedule: Typically, this would be taken once daily.
- Dosing Schedule: Typically, this would be taken once daily.
The math is hypothetical and uses a basic method for conversion. Actual doses would need to be decided through actual studies and not org posts
- Known Side Effects: Minimal sides in animals. Cant be fully certain about sides in humans
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