Drinking alcohol can directly cause dementia, but doctors still do not know exactly how this happens or why some heavy drinkers develop it while others do not. This project will track hundreds of thousands of people across the US, UK, Estonia and China, combining their health records, brain scans, genetic data and blood tests to map the biological pathways that link alcohol to dementia. The researcher has already shown that alcohol is a cause of dementia, not just a risk factor. The problem is that without understanding the underlying mechanisms, clinicians cannot diagnose or treat alcohol-related dementia any differently from other forms. If this work succeeds, it could change how dementia is classified and managed in the clinic. Identifying specific molecular pathways might reveal targets for drugs that could slow or prevent alcohol-driven brain damage. The research is fundamental science — it aims to explain a poorly understood disease mechanism rather than deliver an immediate treatment. But similar work on other dementia risk factors has opened entirely new avenues for therapy, and clarifying how alcohol damages the brain could do the same.
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Alcohol-related dementia has suffered research neglect despite high clinical need. My recent work has found evidence for a causal role of alcohol consumption on dementia, yet lack of pathophysiological knowledge is currently limiting clinical translation of these findings. The research proposed here aims to identify and characterize key pathways by which exposure to alcohol leads to dementia. Clarity of these relationships is vital given the widespread population exposure to alcohol and the lack of disease-modifying treatments for dementia. The key goals are: 1. Examine if alcohol affects risk and course of common and rarer dementia subtypes. 2. Establish whether genetic variation influences the susceptibility of drinkers to dementia. 3. Identify causal molecular pathways driving alcohol’s impact on dementia. I will use a combination of large-scale electronic health records, epidemiological, neuroimaging and multi-omics datasets from the US, UK, Estonia and China. The consequent statistical power will allow triangulation of observational and pseudo-experimental (Mendelian randomization) approaches to improve causal inference. Outcomes: Findings from this work will generate fundamental insights into how alcohol can lead to dementia. I will determine whether dementia with an alcohol aetiology merits specific identification and management. Characterization of molecular pathways will pave the way for potential therapeutic strategies.
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