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Hyperuricemia, Gout, and the Brain-an Update.
Augustin Latourte1,2, Julien Dumurgier3, Claire Paquet3
1Université de Paris, INSERM, UMR-S, 1132 BIOSCAR, 75010, Paris, France. augustin.latourte@aphp.fr.
This review explores the link between uric acid (UA), gout, and brain health. Current evidence suggests UA and gout may not causally impact neurodegenerative diseases or stroke.
Area of Science:
- Neurology
- Rheumatology
- Genetics
Background:
- Hyperuricemia and gout are linked to various health conditions.
- Observational studies suggest complex associations between uric acid levels and brain diseases, including neurodegenerative and cerebrovascular conditions.
- The causal relationship remains unclear.
Purpose of the Study:
- To review current evidence on the relationship between uric acid (UA), gout, and brain diseases.
- To critically evaluate findings from observational and Mendelian randomization (MR) studies.
- To identify gaps in knowledge and suggest future research directions.
Main Methods:
- Systematic review of observational studies and Mendelian randomization (MR) analyses.
- MR studies utilize genetic variants as instrumental variables to infer causality.
- Analysis focused on associations between UA/gout and Alzheimer's disease, dementia, Parkinson's disease, and stroke.
Main Results:
- Observational studies suggest a potential decreased risk of neurodegenerative diseases but an increased risk of cerebrovascular disease in individuals with hyperuricemia or gout.
- MR analyses do not support a causal link between UA or gout and Alzheimer's disease, dementia, or Parkinson's disease.
- MR studies also do not support a causal association between UA and stroke, nor the observed U-shaped association between UA and brain diseases.
Conclusions:
- Current genetic evidence does not support a causal role for uric acid or gout in major brain diseases like Alzheimer's, dementia, or Parkinson's.
- The observed associations in observational studies may not reflect causality.
- Further research is needed to clarify the causal role of gout and the effects of urate-lowering therapies on neurological outcomes.
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