Uncorking the truth

There are no effective treatments for Alzheimer’s disease (AD) and related dementias, and existing interventions require early implementation, before significant pathological accumulation occurs. Because AD pathology often precedes symptoms by several decades, early identification for treatment is challenging. Modifiable risk factors, including lifestyle adjustments, thus represent promising targets for disease prevention. Recent epidemiological studies have highlighted alcohol use as one such risk factor, particularly in early-onset dementia. Though the association between alcohol consumption and AD remains underexplored, both alcohol use and AD pathology have notable impacts on the serotonin system, which may underlie this risk. This dissertation investigates how alcohol exposure may influence AD-like pathology and neuropsychiatric symptoms (NPS), focusing on serotonergic dysfunction as a potential mediator. Understanding how alcohol might accelerate the pathophysiology of dementia could help to identify at-risk individuals for early interventions.