-
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
iNature
Alzheimer's disease (AD) is one of the most common forms of dementia that has no effective clinical treatment
.
On November 17, 2022, Yuan Zengzheng and Pan Ruiyuan of the Military Medical Research Institute jointly published a joint newsletter entitled "Intermittent fasting protects against Alzheimer's disease in mice by altering metabolism through" online in Nature Aging Remodeling of the gut microbiota", which showed that intermittent fasting prevented Alzheimer's in mice by remodeling the gut microbiota to alter metabolism
.
The study revealed that intermittent fasting (IF) improved cognitive function and AD-like pathology
in a transgenic AD mouse model (5XFAD).
IF changes the composition of the intestinal flora, resulting in a significant enrichment of probiotics such as lactic acid bacteria
.
Changes in the composition of the intestinal flora affect metabolic activity and the production
of metabolites.
Metabolomic analysis of cecal contents showed that IF led to decreased carbohydrate metabolism (e.
g.
, glucose) and increased
content of amino acids (e.
g.
, sarcosine and dimethylglycine).
Interestingly, the authors found that sarcosine, or dimethylglycine, which had elevated IF, mimicked the protective effects of IF in 5XFAD mice, including improved cognitive decline, amyloid β (Aβ) burden, and glial overactivation
.
Therefore, the findings suggest that the IF protocol is a potential way to prevent AD progression, at least through the gut-microbiome-metabolite-brain axis, and constitutes an innovative AD therapeutic pathway
.
characterized by memory loss and cognitive impairment.
Deposition of extracellular amyloid-β (Aβ) plaques and formation of intracellular tau nerve fiber tangles are typical pathological features of AD and a major cause
of subsequent neuroinflammation, synaptic damage, neuronal loss, and ultimately cognitive decline.
However, there is growing evidence that these two processes alone cannot fully explain the pathogenesis
of AD.
Over the past few decades, significant efforts to target AD, particularly Aβ, tau protein, neuroinflammation, and other AD-related pathologies, have so far failed to halt or slow the progression
of AD.
The failure of these clinical trials suggests that the pathogenesis of AD may be a systemic disease involving multiple pathways or targets, rather than a simple linear cascade effect intermittent fasting (IF) is a popular approach to dietary restriction with multiple benefits
for human health, aging, and disease.
Emerging evidence suggests that IF is able to prolong life, improve immune function, and improve the pathology
of a wide range of diseases.
Recent studies have shown that IF has a good protective effect
against neurodegenerative diseases including Parkinson's disease and Huntington's disease.
In addition, multiple pieces of evidence suggest that the prognosis
of IF treatment for AD can be improved by reducing AD-related pathologies and cognitive impairment in various AD models.
Still, the mechanism by which IF improves AD is poorly
understood.
IF improved cognitive decline in mice with 5XFAD (Image from Nature Aging), and several studies revealed a correlation
between AD pathology and intestinal dysbacteriosis.
Changes in the composition and diversity of the gut microbiota were observed in AD mouse models and AD patients compared to healthy controls
.
In different mouse models of AD, altering gut microbiota composition and diversity with antibiotics (ABX) or probiotics reduced neuroinflammation and Aβ burden
.
Recent reports have even shown that replacing the gut microbiota with fecal transfer from wild-type (WT) mice is sufficient to improve AD-like lesions
in APP/PS1 and ADLPAPT mice, a newly developed transgenic AD mouse model.
These studies highlight the gut microbiota as a potential therapeutic target for AD therapy
.
Interestingly, there is growing evidence that IF has a significant protective effect
against several diseases, such as obesity, autoimmunity, and diabetes, by regulating the composition of the gut microbiota and microbial metabolism.
Given the growing link between gut microbiota and the pathogenesis of AD, as well as the potential modulatory effect of IF on the gut flora, it is useful
to study the effects of IF on AD and explore the mechanism of action of the gut-microbiome-brain axis in this process.
The study showed that intermittent fasting prevented Alzheimer's disease in mice by altering metabolism by remodeling the gut microbiota
.
The study revealed that intermittent fasting (IF) improved cognitive function and AD-like pathology
in a transgenic AD mouse model (5XFAD).
IF changes the composition of the intestinal flora, resulting in a significant enrichment of probiotics such as lactic acid bacteria
.
Changes in the composition of the intestinal flora affect metabolic activity and the production
of metabolites.
Metabolomic analysis of cecal contents showed that IF led to decreased carbohydrate metabolism (e.
g.
, glucose) and increased
content of amino acids (e.
g.
, sarcosine and dimethylglycine).
Interestingly, the authors found that sarcosine, or dimethylglycine, with elevated IF, mimicked the protective effects of IF in 5XFAD mice, including improved cognitive decline, amyloid β (Aβ) burden, and glial overactivation
.
Therefore, the findings suggest that the IF protocol is a potential way to prevent AD progression, at least through the gut-microbiome-metabolite-brain axis, and constitutes an innovative AD therapeutic pathway
.
Original link: https://doi.
org/10.
1038/s43587-022-00311-y—END—the content is [iNature].
