EFFECT OF ALCOHOL ON LEWY BODY DEMENTIA

Abstract

Lewy Body Dementia (LBD) is a neurodegenerative disorder with complex pathological mechanisms. This scientific review explores the relationship between alcohol consumption and LBD. LBD is characterized by the accumulation of Lewy bodies, and intracellular fibrils containing alpha-synuclein. These contribute to neurodegeneration, affecting cognitive and motor functions. LBD holds substantial prevalence, impacting both cognitive and motor domains. Understanding the potential influence of alcohol on LBD is pivotal due to its widespread societal consumption. The aggregation of alpha-synuclein contributes to neuronal dysfunction and degeneration. Dopaminergic dysfunction is a hallmark of LBD, influencing motor symptoms and contributing to cognitive decline. Disruptions in dopaminergic pathways significantly impact disease progression. Alcohol exhibits a potential to interact with alpha-synuclein, influencing its aggregation and contributing to the neuropathological processes observed in LBD. Alcohols impact extends to neurotransmitter modulation and synaptic dysfunction. Disruptions in these crucial processes may exacerbate the neurodegenerative cascade seen in LBD. Contrastingly, specific components within alcoholic beverages may possess neuroprotective properties, potentially mitigating aspects of LBD pathology. Future directions include the development of the criteria for early diagnosis (prodromal DLB) and the establishment of new biomarkers that directly indicate Lewy-related pathology, including α-synuclein imaging, biopsies of peripheral tissues (skin, etc.) for the demonstration of α-synuclein deposition, and biochemical markers (cerebrospinal fluid/blood), as well as the pathological evaluation of the sensitivity and specificity of the 2017 revised diagnostic criteria.