Nikhil Prasad Fact checked by:Thailand Medical News Team Aug 06, 2024 3 months, 2 weeks, 1 day, 17 hours, 17 minutes ago
Alzheimer’s Disease News: Recent studies have brought to light the significant role that diet plays in the development of Alzheimer's Disease (AD), specifically how a high-fat diet (HFD) can lead to conditions that exacerbate AD. This
Alzheimer’s Disease News report delves into a groundbreaking study conducted by researchers from Texas A&M Health Science Center-USA, which sheds light on how HFD-induced dysregulation of tyrosine kinases can impact the gut-brain axis in Alzheimer's Disease.
New study reveals link between high fat diet and Alzheimer's disease
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Understanding Alzheimer's and the Gut-Brain Axis
The human gastrointestinal tract is home to a vast microbial population that plays a critical role in overall health. Recent research has highlighted the communication between the gut and brain, mediated by gut microbiota and their microbial products, in the pathology of Alzheimer's Disease. AD is a common form of dementia with complex causes, including genetic and lifestyle factors. Notably, a high-fat diet is linked to metabolic syndrome and systemic inflammation, which are significant contributors to AD.
High Fat Diet and Gut Dysbiosis
A high-fat diet induces gut dysbiosis, an imbalance in the gut microbiota, leading to metabolic and systemic inflammation. This dysbiosis results in the disruption of the intestinal barrier, causing chronic low-grade inflammation, obesity, and type-2 diabetes (T2D). These conditions are closely associated with neuroinflammation and the accumulation of Amyloid β (Aβ), a hallmark of AD.
The Role of Janus Kinase 3 (JAK3)
At the molecular level, an HFD causes the dysregulation of Janus kinase 3 (JAK3), a non-receptor tyrosine kinase with significant roles in both the colon and brain. JAK3 is proposed to regulate the phagocytic and migratory functions of microglia, the brain's resident immune cells. The study emphasizes the need for further research to understand the transcription factors linking JAK3 dysregulation to obesity and AD.
Key Findings from the Study
The research team from Texas A&M Health Science Center, including Yomna S. Momen, Jayshree Mishra, and Narendra Kumar, conducted an in-depth review of the literature on HFD and its impact on gut-brain communication. Their findings suggest that transcription factors act as a common language between the gut and brain, regulating JAK3 expression and maintaining intestinal barrier integrity and microglial function. This regulation likely occurs through microglial actin remodeling, which could help alleviate systemic inflammation and Aβ deposition.
Mechanisms of Gut-Brain Communication
The gut-brain communication is complex, involving endocrine, immune, and neuronal mechanisms. The vagus nerve, a major component of this communication, acts as a superhighway carrying information between the gut and brain. The gut&#
39;s intrinsic nervous system, known as the enteric nervous system (ENS), also plays a crucial role. This system is involved in various functions, including immune responses, nutrient detection, and epithelial secretion.
Impact of Gut Microbiota
Gut microbiota significantly influence brain health and disease. Microbial metabolites, such as short-chain fatty acids (SCFAs), produced by the bacterial fermentation of dietary fibers, are vital in this communication. SCFAs, including acetate, propionate, and butyrate, are known to enhance the integrity of the intestinal barrier and have neuroprotective roles. However, an HFD disrupts the balance of these beneficial bacteria, leading to increased gut permeability and systemic inflammation.
Transcription Factors and AD Progression
The study highlights the role of transcription factors in AD progression. High-fat diets dysregulate these factors, leading to increased intestinal permeability and systemic inflammation. Specific transcription factors, such as PPAR-δ, PPARγ, and AMPK, are implicated in obesity and insulin resistance. Dysregulated JAK/STAT signaling pathways also play a crucial role in metabolic diseases and AD.
JAK3 and Epithelial Function
JAK3 is vital for epithelial mucosa functions, including wound healing and maintaining intestinal barrier integrity. An HFD downregulates JAK3 expression, compromising these functions and promoting colonic and systemic inflammation. This downregulation also affects glucose tolerance and insulin receptor interactions, contributing to obesity-associated metabolic syndrome.
Conclusion
The study by Texas A&M Health Science Center researchers provides valuable insights into the mechanisms linking a high-fat diet, gut dysbiosis, and Alzheimer's Disease. Understanding the role of JAK3 and transcription factors in this process opens new avenues for potential therapeutic targets to impede AD progression. The findings underscore the importance of diet in maintaining gut-brain health and preventing neurodegenerative diseases.
The study findings were published in the peer-reviewed journal: Nutrients.
https://www.mdpi.com/2072-6643/16/15/2558
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