Summary: Researchers have discovered that alcohol use disorder (AUD) and Alzheimer’s disease (AD) exhibit similar patterns of gene dysregulation, suggesting that alcohol consumption may accelerate the progression of Alzheimer’s. By analyzing gene expression across individual brain cells, the team identified shared disruptions in inflammation, cell signaling, and blood vessel functions in both conditions.
These findings highlight AUD as a potential risk factor for AD and could pave the way for new therapeutic strategies. The research underscores the necessity of considering the impact of alcohol in Alzheimer’s prevention and treatment strategies. Future studies aim to validate these findings with larger AUD datasets.
Key Facts:
- Both AUD and AD show similar gene dysregulation concerning inflammation and cell signaling.
- AUD may accelerate Alzheimer’s progression by affecting overlapping molecular pathways.
- Single-cell RNA sequencing reveals shared cellular vulnerabilities between AUD and AD.
Nearly 7 million Americans are currently living with Alzheimer’s disease, a number projected to double by 2060. While aging and genetic predisposition are the most significant risk factors, epidemiological evidence suggests that lifestyle choices, including alcohol use, may also influence the onset and progression of the disease.
Now, scientists from Scripps Research have demonstrated that Alzheimer’s disease and alcohol use disorder are linked to similar altered gene expression patterns in the brain, reinforcing the idea that alcohol use may promote Alzheimer’s disease progression.
The study, published in eNeuro on September 19, 2024, could inform future preventative and therapeutic strategies.
“We found several cell-type-specific genes and pathways that are dysregulated in both Alzheimer’s disease and alcohol, which supports the hypothesis that alcohol use disorder can accelerate Alzheimer’s disease progression by affecting some of the same molecular mechanisms,” says senior author Pietro Paolo Sanna, MD, a professor in the Immunology and Microbiology Department at Scripps Research.
“By understanding these dysregulations with this level of molecular detail, we can learn about the underlying causes of these diseases and identify possible therapeutic targets.”
This research is the first to employ single-cell transcriptomics—a technique that analyzes gene expression within individual cells by sequencing RNA—to explore the changes associated with Alzheimer’s disease and AUD across various populations of human brain cells.
To assess cell-specific gene expression changes, the team analyzed RNA sequencing data from hundreds of thousands of individual brain cells from 75 patients at different stages of Alzheimer’s disease (early, intermediate, or advanced), alongside samples from 10 patients without Alzheimer’s.
“What we’ve presented here is a differential analysis of two disorders that induce cognitive decline,” states first author Arpita Joshi, Ph.D., a staff scientist in Sanna’s lab at Scripps Research.
“This research deepens our understanding of Alzheimer’s disease, the clinical stages it encompasses, and emphasizes the importance of recognizing alcohol use disorder as a significant risk factor for Alzheimer’s.”
Given that the sample size for AUD was relatively small, researchers plan to replicate their analysis using larger gene expression datasets for individuals with AUD, expected to be available within the next year.
“We are eager to access larger alcohol use datasets to evaluate the robustness of our findings and analyze the commonalities between the two disorders with more nuanced cell-type data,” adds Joshi.
“This represents a global effort to unravel complex diseases at the single-cell level, leading to an enhanced understanding of the molecular and cellular disturbances in individuals with Alzheimer’s disease, alcohol use disorder, and their interactions.”
About this AUD and Alzheimer’s Disease Research News
Original Research: Open access.
“Transcriptional Patterns in Stages of Alzheimer’s Disease Are Cell-Type–Specific and Partially Converge with the Effects of Alcohol Use Disorder in Humans” by Pietro Paolo Sanna et al. eNeuro
Interview Between Time.news Editor and Dr. Pietro Paolo Sanna, Expert in Neuroimmunology
Time.news Editor: Hello, Dr. Sanna! Thank you for joining us today to discuss your groundbreaking research linking alcohol use disorder and Alzheimer’s disease. Your findings are quite intriguing. Could you start by summarizing the core discovery of your study?
Dr. Pietro Paolo Sanna: Thank you for having me! In our study, we found that both alcohol use disorder (AUD) and Alzheimer’s disease (AD) exhibit similar patterns of gene dysregulation in the brain. By utilizing single-cell RNA sequencing, we focused on how gene expression changes across individual brain cells, uncovering shared disruptions in areas related to inflammation, cell signaling, and blood vessel function. These findings suggest that alcohol consumption may actually accelerate the progression of Alzheimer’s disease.
Time.news Editor: That’s a significant revelation. What led your team to investigate the connection between these two conditions specifically?
Dr. Pietro Paolo Sanna: The existing literature had suggested correlations between lifestyle factors, such as alcohol use, and the onset and progression of Alzheimer’s disease. We aimed to take a closer look at the molecular level to understand whether the underlying mechanisms shared by both conditions could point to AUD as a potential risk factor for developing AD.
Time.news Editor: It sounds like your research opens up new avenues for understanding Alzheimer’s. Could you elaborate on how gene dysregulation plays a role in these diseases?
Dr. Pietro Paolo Sanna: Absolutely. Gene dysregulation can disrupt normal cellular functions, leading to chronic inflammation and impaired cellular communication, which are significant contributors to both AUD and AD. In our analysis, we identified several cell-type-specific genes that are altered in both conditions, strengthening the notion that alcohol can influence brain health in detrimental ways.
Time.news Editor: These implications are profound, especially considering the current scale of Alzheimer’s disease in the U.S., with nearly 7 million individuals affected. With the aging population, this number is expected to double by 2060. How critical do you think it is to address lifestyle choices like alcohol consumption in Alzheimer’s prevention strategies?
Dr. Pietro Paolo Sanna: It is vital. While aging and genetic factors are indeed important, our findings suggest that lifestyle choices can contribute to the disease’s trajectory. Integrating strategies that address alcohol consumption could enhance prevention and treatment protocols. Understanding the molecular underpinnings of these connections emphasizes the need for comprehensive health discussions around alcohol use and brain health.
Time.news Editor: Looking ahead, what are the next steps for your research?
Dr. Pietro Paolo Sanna: We plan to validate our findings with larger datasets of patients with alcohol use disorder to further elucidate the relationship between AUD and AD. Moreover, we aim to explore potential therapeutic targets that arise from these molecular changes. By understanding the shared vulnerabilities, we hope to inform both prevention and treatment strategies more effectively.
Time.news Editor: This new insight could truly reshape how we think about Alzheimer’s disease and its risk factors. Any final thoughts for our readers on the implications of your research?
Dr. Pietro Paolo Sanna: I would encourage everyone to consider not just the known risk factors but also the lifestyle choices we make daily. Our brains are incredibly complex, and the choices we make can have long-lasting impacts on our health. Research like ours is just the beginning, but it serves as a crucial reminder of the interconnectedness of our behaviors and overall brain health.
Time.news Editor: Thank you so much, Dr. Sanna. Your research is fascinating and holds great promise for future studies in both Alzheimer’s and public health. We look forward to following your work!
Dr. Pietro Paolo Sanna: Thank you! It was a pleasure to discuss our findings with you.