A new review suggests how the food patterns increase a range of reactions in your intestine and brain that can help prevent Alzheimer’s, Parkinson’s and other neurodynative diseases.

Study: Stopped as a neuroprotective strategy: intestinal -brain axia and metabolism in neurodynative disordersImage Credit: Chizhevskaya Ekaterina/Shutterstock.com

A review published in Nutrients The existing pre -pregnant and limited clinical evidence was examined, shown that intermittent fasting (IF) can help reduce the burden of toxic protein, support synaptic functions, and rehabilitate glial and immune homeostasis in the models of various neurodogenative disorders.

Intermittent fasting and intestine-brain axis

Research has connected that if up to high levels of bacteria known to produce beneficial metabols and regulate immune responses. In these metabolites, short-chain fatty acids (SCFAs) are important signaling molecules in the intestinal-brain axis (GBA), and the current evidence indicates the role of if IF IF SCFA-productive to increase bacteria, such as Vobacterium Rectel, Rosaburia SPP. And Enarostips SPP. Preclinical studies have paired it with increased hippocampus synaptic density and low tau Protein phosphorization In the animal model of Alzheimer’s disease (Edd).

If the microbial genes upgrade the expression, especially enhances the development of butter-producing taxes. It also modifies biliary acid metabolism and controls the triptophan routes, which improves the production of neuromodulatory metabolites, Easy, serotonin and curnin. If it is associated with a decline in broadcasting monocytes, which are extremely important in the body’s inflammatory reaction.

Chronic lower grade Swelling And provoking from the intestine is rapidly recognized as major factors in neurodizonation. The intestinal permeability, also known as “tapki intestine”, allows microbial endotoxin to enter systemic circulation, trigger immune responses and produce pregnancy cytokins. If SCFA-producers can increase microbes, epithelial integrity can improve and reduce endotoxin exposure.

Recent findings suggest that if the neurotransmitter that occurs in the intestine affects the routes, especially in triptophyne and serotonin metabolism. If under conditions, indol derivatives have more microbial conversion of triptophyne, which can provide neuroprotective benefits via the Aril hydrocarbon receptor (AHR) signaling. It can also support balance between intestines and immune functions.

Neuroinflamation is circadian-sensitive, where hypothalamic inflammation may increase in the case of incorrectly fed schedules. If hypothalamic lipoclyn -2 reduces expression, the hypothalamic restores homeostasis, and increases astrocytic clearance pathway. If the effect on circadian rhythm can also affect redox homeostasis in the brain and can change mitochondrial mobility.

Metabolic reprograming, neuroprootetenance and intermittent fasting

If lipids and ketone-based substrates from glucose, such as β-hydroxybutyrate (BHB) such as metabolic switching can increase mitochondrial efficiency and antioxidant capacity. BHB has a neuroprotective effect through its antioxidant defense, modulation of mitochondrial function and GBA. BHB has preserved mitochondrial membrane capacity in pre -pricly models and improves cognitive performance in AD and epilepsy. BHB contributes to intestine health by strengthening the integrity of intestinal obstruction. Merusing BHB with GBA and provides a strong framework if oxidative stress and increase mitochondrial bioenegotics.

If it activates the autofai by activating Sirt1 and disrupts the mechanical target of rapamycin (MTOR). The SCFAS is also shown to affect the epigenetic regulation of the autofagi genes. Emotional brain-rich neurotrophic factor (BDNF) expression, low amyroid plaque burden, and tau hyperphosphoresilation in the AD model, as well as similar effects have been noted in the model of Parkinson’s disease.

The existing research on neuroimmune interaction has shown that if glial -neuronal interaction and blood -brain controls the integrity of the obstruction. If the GBA-integrated signals affect neuroimmune homeostasis that regulates glial activity, cytokine network and immune-metabolic flexibility. These adaptations are important for long -term cognitive protection and neuroprootetenance.

Clinical practice and translation in future directions

To translate the promise of clinical practice requires a complete inquiry from mechanically monitoring, safety, privatization and moral deployment. Due to the risk of hypoglyciamia, dehydration, and micronutrient deficiencies, it can be difficult to deploy to interfere with weaker population such as older adults. The adherence can also be challenging, especially when cognitive decline obstructs regular maintenance, if it becomes unsafe when possible. Careful compliance platforms, app-directed timers and other digital solutions can bridge this difference.

A change towards the exact fast is emerging, guided by growing evidence that genetic, epigenetic, metabolomic, and Microbiom-The relative factors shape individual reactions for fasting. The inclusion of the circadian biomarker, such as melatonin rhythm, sleep phase, and cortisol dimensions, provides a promising route for individual chrono nutrition. This approach can be particularly beneficial for individuals with neurodygenettive disorders, which often experience disrupting circadian rhythms.

If pelotropic effects make it an ideal backbone for multimodal therapeutic coordination. This is important in the case of neurodizonation, where a monotheraputic approach is unlikely to long lasting clinical benefits. Aerobic or resistance training co-administration and if some pre-pregnant and pilot clinical studies have received adative neurocogical benefits.

If a potential scalable is emerging as a neurotheraputic strategy. As a progress of clinical applications, a comprehensive precision should be concentrated if included in the drug structure. This can be done using digital health technologies, multi-ommics biomarkers and supplementary treatments. However, it is necessary to note that currently most auxiliary evidences come from pre -pricly animal studies, and strong, massive human testing are still limited.

Future research that conducts random controlled tests should adopt stratification designs, integrate longitudinal biomarkers, and consider the real world rearing.

Now download your PDF copy!