-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
- Cosmetic Ingredient
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
As the average life expectancy increases and the fertility rate decreases, the world’s “ageing” speed has accelerated significantly since the 21st century.
With the increase of the elderly, the incidence of age-related cognitive decline and neurodegenerative diseases caused by inflammation, neurobiological changes, diet and lifestyle, etc.
is also increasing.
Studies have shown that reducing the essential amino acid methionine (Met) in the diet, that is, methionine restriction (MR), can extend the lifespan of yeast, fruit flies and rodents, reduce oxidative damage and change the lipid composition in the brain, and strengthen neurons The vitality improves the memory impairment of obese mice induced by high-fat diet (HFD).
However, whether MR has a protective effect on age-related cognitive decline and its underlying mechanism are still unclear.
Recently, researchers from Northwest A&F University in my country published a study titled Methionine restriction alleviates age-associated cognitive decline via fibroblast growth factor 21 in "Redox Biology".
They found that methionine restriction can be increased by activating the nutritional factor FGF21.
Significantly improve the cognitive decline associated with neurodegenerative diseases.
https://doi.
org/10.
1016/j.
redox.
2021.
101940 In order to clarify whether MR has a protective effect on cognitive function, the researchers performed a three-month experiment on mice of two months, one year, and fifteen months.
MR diet processing, and detection of body weight, lipids and other physical indicators, and at the same time through Morris water maze, object recognition and other behavioral tests to evaluate the cognitive ability of mice.The results found that compared with control mice, MR significantly improved the cognitive impairment caused by age in 15-month-old and 18-month-old mice (initial ages were 12 months and 15 months), and restored their aging-related impairments.
Spontaneous changes and the reduction of the object recognition test index also shorten the escape latency.
Methionine restriction reduces cognitive impairment in the hippocampus of aged mice is the neural basis of cognitive function.
The researchers found by staining the hippocampus of mice that MR inhibited neuronal degeneration in the dentate gyrus of aged mice.
Later, the ultrastructure and mitochondrial morphology of hippocampal synapses in 5, 15 and 18-month-old mice were examined by transmission electron microscopy.
Further evaluation to study the effect of MR on synaptic function.
The results showed that although MR had no effect on the postsynaptic density of 5-month-old mice, it significantly improved hippocampal synaptic ultrastructure and mitochondrial biogenesis in 15- and 18-month-old mice, resulting in PSD length and broadband Increased, the expression of essential structural protein Psd95 increased, and the ratio of abnormal mitochondria to normal mitochondria decreased.
The restriction of methionine improved the ultrastructure of synapses in the hippocampus of aged mice and changed the biogenesis of mitochondria.
To further investigate how MR regulates these important biological pathways in the brain, the researchers performed transcriptome sequencing on the hippocampus of mice After analysis, it was found that the gene expression patterns of 18-month-old control mice and MR mice were opposite.
In the hippocampus of aging MR mice, fibroblast growth factor 1 (Fgfr1) and its receptors increased with age.
The expression level of the somatic complex β-klotho was down-regulated, and the expression of fibroblast growth factor 21 (FGF21), which decreased with age, was significantly activated, and the expression of other hippocampal neural structure-related genes was also affected.
Since inflammation and oxidative homeostasis are also closely related to neuronal cell function and cognitive function, the researchers tested the inflammatory cytokines and oxidation markers in the hippocampus of MR mice and found that MR reduced the rise of inflammatory factors caused by aging.
At the same time, it activates the antioxidant defense system and also reduces the levels of lipid peroxidation products and oxidative damage markers in the cortex of aging mice.
In addition, it was also observed through the mitochondrial membrane potential that FGF21 improved the oxidative stress of nerve cells.
This indicates that FGF21 may be a molecular target that mediates the neuroprotective function of MR.
After MR-mediated improvement of cognitive impairment in elderly mice requires FGF21, the researchers constructed a knock-out of Fgf21 in aging mice to further explore whether the neuroprotective function of MR requires FGF21 activation.
After performing behavioral sequencing, PSD observation, oxidative stress and inflammation level detection in mice, it was found that FGF21 plays a key role in improving age-related cognitive deficits.
It can activate Nrf2 signaling and reduce neuroinflammation and oxidative stress.
, The knockout of FGF21 in mice also reduced the length and width of PSD, and the improvement of cognitive function by MR was also partially eliminated.
In short, the study found that MR can further protect synaptic ultrastructure and enhance mitochondrial biogenesis genes, inhibit neuroinflammation and oxidative damage by activating circulating FGF21, thereby improving cognitive ability.
The results may help to develop new dietary strategies to combat aging and cognitive decline inherent in certain neurodegenerative diseases, and obtain considerable clinical value.
End reference materials: [1]
With the increase of the elderly, the incidence of age-related cognitive decline and neurodegenerative diseases caused by inflammation, neurobiological changes, diet and lifestyle, etc.
is also increasing.
Studies have shown that reducing the essential amino acid methionine (Met) in the diet, that is, methionine restriction (MR), can extend the lifespan of yeast, fruit flies and rodents, reduce oxidative damage and change the lipid composition in the brain, and strengthen neurons The vitality improves the memory impairment of obese mice induced by high-fat diet (HFD).
However, whether MR has a protective effect on age-related cognitive decline and its underlying mechanism are still unclear.
Recently, researchers from Northwest A&F University in my country published a study titled Methionine restriction alleviates age-associated cognitive decline via fibroblast growth factor 21 in "Redox Biology".
They found that methionine restriction can be increased by activating the nutritional factor FGF21.
Significantly improve the cognitive decline associated with neurodegenerative diseases.
https://doi.
org/10.
1016/j.
redox.
2021.
101940 In order to clarify whether MR has a protective effect on cognitive function, the researchers performed a three-month experiment on mice of two months, one year, and fifteen months.
MR diet processing, and detection of body weight, lipids and other physical indicators, and at the same time through Morris water maze, object recognition and other behavioral tests to evaluate the cognitive ability of mice.The results found that compared with control mice, MR significantly improved the cognitive impairment caused by age in 15-month-old and 18-month-old mice (initial ages were 12 months and 15 months), and restored their aging-related impairments.
Spontaneous changes and the reduction of the object recognition test index also shorten the escape latency.
Methionine restriction reduces cognitive impairment in the hippocampus of aged mice is the neural basis of cognitive function.
The researchers found by staining the hippocampus of mice that MR inhibited neuronal degeneration in the dentate gyrus of aged mice.
Later, the ultrastructure and mitochondrial morphology of hippocampal synapses in 5, 15 and 18-month-old mice were examined by transmission electron microscopy.
Further evaluation to study the effect of MR on synaptic function.
The results showed that although MR had no effect on the postsynaptic density of 5-month-old mice, it significantly improved hippocampal synaptic ultrastructure and mitochondrial biogenesis in 15- and 18-month-old mice, resulting in PSD length and broadband Increased, the expression of essential structural protein Psd95 increased, and the ratio of abnormal mitochondria to normal mitochondria decreased.
The restriction of methionine improved the ultrastructure of synapses in the hippocampus of aged mice and changed the biogenesis of mitochondria.
To further investigate how MR regulates these important biological pathways in the brain, the researchers performed transcriptome sequencing on the hippocampus of mice After analysis, it was found that the gene expression patterns of 18-month-old control mice and MR mice were opposite.
In the hippocampus of aging MR mice, fibroblast growth factor 1 (Fgfr1) and its receptors increased with age.
The expression level of the somatic complex β-klotho was down-regulated, and the expression of fibroblast growth factor 21 (FGF21), which decreased with age, was significantly activated, and the expression of other hippocampal neural structure-related genes was also affected.
Since inflammation and oxidative homeostasis are also closely related to neuronal cell function and cognitive function, the researchers tested the inflammatory cytokines and oxidation markers in the hippocampus of MR mice and found that MR reduced the rise of inflammatory factors caused by aging.
At the same time, it activates the antioxidant defense system and also reduces the levels of lipid peroxidation products and oxidative damage markers in the cortex of aging mice.
In addition, it was also observed through the mitochondrial membrane potential that FGF21 improved the oxidative stress of nerve cells.
This indicates that FGF21 may be a molecular target that mediates the neuroprotective function of MR.
After MR-mediated improvement of cognitive impairment in elderly mice requires FGF21, the researchers constructed a knock-out of Fgf21 in aging mice to further explore whether the neuroprotective function of MR requires FGF21 activation.
After performing behavioral sequencing, PSD observation, oxidative stress and inflammation level detection in mice, it was found that FGF21 plays a key role in improving age-related cognitive deficits.
It can activate Nrf2 signaling and reduce neuroinflammation and oxidative stress.
, The knockout of FGF21 in mice also reduced the length and width of PSD, and the improvement of cognitive function by MR was also partially eliminated.
In short, the study found that MR can further protect synaptic ultrastructure and enhance mitochondrial biogenesis genes, inhibit neuroinflammation and oxidative damage by activating circulating FGF21, thereby improving cognitive ability.
The results may help to develop new dietary strategies to combat aging and cognitive decline inherent in certain neurodegenerative diseases, and obtain considerable clinical value.
End reference materials: [1]
