Background: Dementia is a globally increasing health issue and since no cure is currently available, prevention is crucial. The consumption of alcohol is a controversially discussed risk factor for dementia. While many previously published epidemiological studies reported a risk reduction by light to moderate alcohol consumption, there is no persuasive model of an underlying biochemical mechanism. The purpose of this article is to review current models on alcohol neurotoxicity and dementia and to analyze and compare studies focusing on the epidemiological link between alcohol consumption and the risk of dementia. Methods: The electronic database Pubmed was searched for studies published between 1994 and 2019 concerning the topic. Results: Available epidemiological studies are not sufficient to verify a protective effect of alcohol on dementia development.

Defects in intracellular transport are implicated in the pathogenesis of Alzheimer’s disease (AD). Hook proteins are a family of cytoplasmic linker proteins that participate in endosomal transport. In this study we show that Hook1 and Hook3 are expressed in neurons while Hook2 is predominantly expressed in astrocytes. Furthermore, Hook proteins are associated with pathological hallmarks in AD; Hook1 and Hook3 are localized to tau aggregates and Hook2 to glial components within amyloid plaques. Additionally, the expression of Hook3 is reduced in AD. Modelling of Hook3 deficiency in cultured cells leads to slowing of endosomal transport and increases β-amyloid production. We propose that Hook3 plays a role in pathogenic events exacerbating AD.