Abstract

Cognitive reserve (CR) is the capability of an individual to cope with a brain pathology through compensatory mechanisms developed through cognitive stimulation by mental and physical activity. Recently, it has been suggested that CR has a protective role against the initiation of substance use, substance consumption patterns and cognitive decline and can improve responses to treatment. However, CR has never been linked to cognitive function and neurotrophic factors in the context of alcohol consumption. The present cross-sectional study aims to evaluate the association between CR (evaluated by educational level), cognitive impairment (assessed using a frontal and memory loss assessment battery) and circulating levels of brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) in patients with alcohol use disorder (AUD). Our results indicated that lower educational levels were accompanied by earlier onset of alcohol consumption and earlier development of alcohol dependence, as well as impaired frontal cognitive function. They also suggest that CR, NT-3 and BDNF may act as compensatory mechanisms for cognitive decline in the early stages of AUD, but not in later phases. These parameters allow the identification of patients with AUD who are at risk of cognitive deterioration and the implementation of personalized interventions to preserve cognitive function.

Highlights

  • Cognitive reserve (CR) is the capability of an individual to cope with a brain pathology through compensatory mechanisms developed through cognitive stimulation by mental and physical activity

  • Cognitive impairment and neurotrophic factors have been widely described in the scientific literature; they have never been linked in an integrated way with cognitive reserve and education level

  • Education level is known to be a robust measure of cognitive reserve that contributes to delaying and smoothing the progress of mild cognitive impairment and other neurodegenerative p­ athologies[13,16]

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Summary

Introduction

Cognitive reserve (CR) is the capability of an individual to cope with a brain pathology through compensatory mechanisms developed through cognitive stimulation by mental and physical activity. Our results indicated that lower educational levels were accompanied by earlier onset of alcohol consumption and earlier development of alcohol dependence, as well as impaired frontal cognitive function. They suggest that CR, NT-3 and BDNF may act as compensatory mechanisms for cognitive decline in the early stages of AUD, but not in later phases. High alcohol consumption has been associated with an acceleration of cognitive decline in a­ ging[3], the WHO considers alcohol consumption to be one of the many risk factors for dementia and not a main component in the etiology of the disease. It has been shown that a high education level softens the clinical manifestations and the progression of mild cognitive impairment[13]; in addition, it has been related to fewer alterations in the biomarkers t-tau, p-tau, t-tau/AB42, and p-tau/AB42 in individuals with Alzheimer’s ­disease[14]

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