Summary: A new study sheds light on the potential role of diet in preventing dementia. The analysis explored the relationship between gut health and Alzheimer’s disease, uncovering a strong link between specific types of gut bacteria and the likelihood of developing dementia.
The findings highlight the significance of gut microbiota in brain health and provide insights into the underlying mechanisms of Alzheimer’s disease.
This research opens up new avenues for personalized treatments and interventions that target gut health to potentially slow down or prevent the development of dementia.
The study found a significant correlation between 10 specific types of gut bacteria and the likelihood of developing Alzheimer’s disease. Six of these bacteria were identified as protective, while four were identified as risk factors for the disease.
Certain bacteria in the human gut can secrete acids and toxins that interact with the APOE gene, a major risk factor for Alzheimer’s disease, triggering a neuroinflammatory response that can affect brain health and immune functions.
The analysis revealed that an imbalance of gut bacteria can have negative effects on the immune system and is linked to various diseases, including depression, heart disease, cancer, and Alzheimer’s disease. This highlights the importance of maintaining a healthy balance of gut microbiota for overall health and disease prevention.
Source: University of Nevada Las Vegas
Could changing your diet play a role in slowing or even preventing the development of dementia? We’re one step closer to finding out, thanks to a new UNLV study that bolsters the long-suspected link between gut health and Alzheimer’s disease.
The analysis — led by a team of researchers with the Nevada Institute of Personalized Medicine (NIPM) at UNLV and published this spring in the Nature journal Scientific Reports — examined data from dozens of past studies into the belly-brain connection. The results? There’s a strong link between particular kinds of gut bacteria and Alzheimer’s disease.
Between 500 and 1,000 species of bacteria exist in the human gut at any one time, and the amount and diversity of these microorganisms can be influenced by genetics and diet.
The UNLV team’s analysis found a significant correlation between 10 specific types of gut bacteria and the likelihood of developing Alzheimer’s disease. Six categories of bacteria — Adlercreutzia, Eubacterium nodatum group, Eisenbergiella, Eubacterium fissicatena group, Gordonibacter, and Prevotella9 — were identified as protective, and four types of bacteria — Collinsella, Bacteroides, Lachnospira, and Veillonella — were identified as a risk factor for Alzheimer’s disease.
Certain bacteria in humans’ guts can secrete acids and toxins that thin and seep through the intestinal lining, interact with the APOE (a gene identified as a major risk factor for Alzheimer’s disease), and trigger a neuroinflammatory response — affecting brain health and numerous immune functions, and potentially promoting development of the neurodegenerative disorder.
Researchers said their novel discovery of the distinct bacterial groups associated with Alzheimer’s disease provides new insights into the relationship between gut microbiota and the world’s most common form of dementia. The findings also advance scientists’ understanding of how an imbalance of that bacteria may play a role in the disorder’s development.
“Most of the microorganisms in our intestines are considered good bacteria that promote health, but an imbalance of those bacteria can be toxic to a person’s immune system and linked to various diseases, such as depression, heart disease, cancer, and Alzheimer’s disease,” said UNLV research professor Jingchun Chen.
“The take-home message here is that your genes not only determine whether you have a risk for a disease, but they can also influence the abundance of bacteria in your gut.”
While their analysis established overarching categories of bacteria typically associated with Alzheimer’s disease, the UNLV team said further research is needed to drill down into the specific bacterial species that influence risk or protection.
The hope is to one day develop treatments that are customized for an individual patient and their genetic makeup, such as medications or lifestyle change.
Studies have shown that changes in gut microbiome through probiotic use and dietary adjustments can positively impact the immune system, inflammation, and even brain function.
“With more research it would be possible to identify a genetic trajectory that could point to a gut microbiome that would be more or less prone to developing diseases such as Alzheimer’s,” said study lead author and UNLV graduate student Davis Cammann, “but we also have to remember that the gut biome is influenced by many factors including lifestyle and diet.”
Genetic correlations between Alzheimer’s disease and gut microbiome genera
A growing body of evidence suggests that dysbiosis of the human gut microbiota is associated with neurodegenerative diseases like Alzheimer’s disease (AD) via neuroinflammatory processes across the microbiota-gut-brain axis.
The gut microbiota affects brain health through the secretion of toxins and short-chain fatty acids, which modulates gut permeability and numerous immune functions. Observational studies indicate that AD patients have reduced microbiome diversity, which could contribute to the pathogenesis of the disease.
Uncovering the genetic basis of microbial abundance and its effect on AD could suggest lifestyle changes that may reduce an individual’s risk for the disease.
Using the largest genome-wide association study of gut microbiota genera from the MiBioGen consortium, we used polygenic risk score (PRS) analyses with the “best-fit” model implemented in PRSice-2 and determined the genetic correlation between 119 genera and AD in a discovery sample (ADc12 case/control: 1278/1293).
To confirm the results from the discovery sample, we next repeated the PRS analysis in a replication sample (GenADA case/control: 799/778) and then performed a meta-analysis with the PRS results from both samples.
Finally, we conducted a linear regression analysis to assess the correlation between the PRSs for the significant genera and the APOE genotypes. In the discovery sample, 20 gut microbiota genera were initially identified as genetically associated with AD case/control status.
Of these 20, three genera (Eubacterium fissicatena as a protective factor, Collinsella, and Veillonella as a risk factor) were independently significant in the replication sample. Meta-analysis with discovery and replication samples confirmed that ten genera had a significant correlation with AD, four of which were significantly associated with the APOE rs429358 risk allele in a direction consistent with their protective/risk designation in AD association.
Notably, the proinflammatory genus Collinsella, identified as a risk factor for AD, was positively correlated with the APOE rs429358 risk allele in both samples. Overall, the host genetic factors influencing the abundance of ten genera are significantly associated with AD, suggesting that these genera may serve as biomarkers and targets for AD treatment and intervention.
Our results highlight that proinflammatory gut microbiota might promote AD development through interaction with APOE. Larger datasets and functional studies are required to understand their causal relationships.