Summary: Kaempferol, a natural antioxidant found in foods like spinach and berries, may aid in the protection of brain cells and has potential as a remedy for ALS and memory. According to research, it increases energy production and reduces stress in muscle tissue, aiding in maintaining muscle function and preventing degeneration.
Yet, the body only absorbs flavonoids, so large amounts may be required for therapeutic effects from diet alone. Scientists are currently developing lipid-based nanoparticles to improve the ability of the substances to reach the brain and nervous system.
Important Information
- KAEPPERFEROL: A KAEEPPEROL promotes energy production and reduces body tension in ALS-affected neurons.
- Absorption Challenge: The body’s inability to absorb nutrition flavonoids limits its healing potential.
- To boost absorption and goal neurons, researchers want to embody kaempferol in fatty nanoparticles.
University of Missouri supply
According to new research from the University of Missouri, a natural substance found in common fruits and vegetables may hold the key to protecting muscle tissue.
Smita Saxena, a teacher of natural remedies and treatment at the School of Medicine and cause author of the study, said,” It’s fascinating to discover a naturally occurring substances that may help people suffering from ALS or dementia.”
We discovered that this substance had a significant influence on both maintaining motors and muscle function and reducing muscle atrophy.
The study found that flavonoid, a natural antioxidants found in kale, berries, and endives, may help the health of nerve cells and has potential as a possible treatment for ALS.
The compound, which was grown in lab-grown brain cells from ALS patients, increased the cells ‘ production of energy and lessened stress in the cellular reticulum, which processes proteins. Also, the substance enhanced nerve cell damage and general body function.
Researchers discovered that flavonoids succeeded by reversing a vital pathway that aids in energy production and protein management, two processes that are hampered by ALS.
According to Saxena,” I think this is one of the primary compounds that can simultaneously target both the cellular reticulum and mitochondria.” It has the ability to have a potent neurotoxic effect by interfering with both of these components within muscle cells.
The difficulty
The find? Kaempferol is not easily absorbed by the body, and it might take a lot to see true rewards in people. For example, to get a helpful dose of kale, an ALS patient would need to consume at least 10 to 11 pounds of it each day.
Our body don’t absorb flavonoid from the vegetables we consume, Saxena said.
Because of this, only a small portion of our cells are affected, which limits its potency. We need to enhance or change the amount of kaempferol so that it can be absorbed more easily.
Another challenge is introducing the mixture into the mind. A strongly encircled layer of cells that prevents harmful substances makes it harder for larger molecules like flavonoid to pass through the blood-brain hurdle.
What comes future?
Despite its difficulties, flavonoids continues to be a promising treatment for ALS, especially since it continues to work even after symptoms begin to manifest. It also shows potential for other neurodegenerative diseases including Alzheimer’s and Parkinson’s.
Saxena’s staff at the Roy Blunt NextGen Precision Health tower is looking at ways to increase its adoption by cells to make the mixture easier for the body to digest.
One promising method involves packaging small spherical particles made of fats, which are frequently used in medication delivery, into lipid-based nanoparticles.
The goal is to represent flavonoids within lipid-based nanoparticles that are readily absorbed by the cells, Saxena said.  ,
” This had target kaempferol to cells in a way that would significantly increase its valuable effect.”
The team is currently developing the particles, hoping to have them tested by the year’s end.
About this study on Und and Alzheimer’s disease.
Publisher: Sara Diedrich
Source: University of Missouri
Contact: Sara Diedrich – University of Missouri
Image: The image is credited to Neuroscience News
Start access to original study.
Smita Saxena and colleagues ‘ study” Kaempferol protects motor neurons from mitochondrial function and ER strain in C9ORF72-ALS and enhances ER-mitochondria linkage..” Acta Neuropathologica Communications
Abstract
Kaempferol protects motor neurons from mitochondrial function and ER strain in C9ORF72-ALS and enhances ER-mitochondria linkage.
Repeat expansions in the genes C9ORF72 and C9ORF72 are a frequent cause of frontotemporal dementia and amyotrophic lateral sclerosis ( ALS ) in people. Significant progress has been made in identifying and treating C9ORF72-mediated illness and resolving its actual etiopathogenesis.
The involvement of persistent cellular reticulum stress and intrinsic mitochondrial deficits in the development of the C9ORF72-linked pathology is well established.
No treatment or powerful treatment has yet to be discovered, so efforts to find a potential drug target have gained more and more attention.
In preliminary squirrel and animal models of the disease C9ORF72-ALS, we examined the mode of action and healing effect of a naturally occurring eating flavanol, kaempferol.
Importantly, kaempferol treatment of , C9ORF72-ALS people patient-derived engine neurons/neurons resolved nuclear deficits, promoted endurance against extreme ER stress, and conferred neuroprotection.
Treatment of symptomatic C9ORF72 mice with flavonoid resulted in adjusted nuclear calcium uptake, restored mitochondrial function, and reduced ER stress.
Interestingly, chronic kaempferol administration improved pathological motor dysfunction and hindered motor neuron degeneration in vivo, demonstrating the potential of kaempferol’s translational effects.
Finally, in-silico modeling demonstrated a book kaempferol target, and biologically the iP3R-VDAC1 pathway’s GRP75 expression modulation serves as the kaempferol’s neuroprotective mechanism.
So, kaempferol holds a lot of promise for treating neurological conditions where both mtdna and ER function are intrinsically related to the pathophysiology.
