CO09 | Homocysteine: marker of neurodegeneration in patients with alcohol dependence syndrome

M. Cola, P.L. Pujatti | Ospedale Cazzavillan, Via del parco 1 Arzignano (VI), Italy

Aims: Alcoholism correlates with increased homocysteine, whose metabolism requires vitamins B12, B6, and B9 as cofactors. Homocysteine overcomes BBB by acting as a neurotoxin, promoting demyelination, leading to up-regulation of NMDA receptors, glutamate accumulation and neuronal lipid peroxidation, cellular changes underlying phenomena such as learning, memory and dysesthesia. The study assesses the association between hyperhomocysteinemia in alcoholics and central/peripheral neuronal damage.
Methods: MOCA and MMSE psychometric instruments, EMG. Results: 45 patients underwent homocysteine assays at enrollment found to be above threshold values in 96% of cases; at T0 performed neurocognitive assessment by MOCA and MMTE with mild to moderate impairment of cognitive abilities in 65% of cases. EMG performed at T0 documented mild signs of neurogenic distress in 30% of patients. After a course of parenteral B vitamins and continued vitamin oral supplementation for 6 month repeat tests were performed providing improvement in cognitive abilities in 85% of cases: moderate/light to mild. Repeat EMG at 6 months was also negative in 20% of patients with mild signs of distress. Homocysteine values at T6 were in range in 99% of patient.
Conclusions: Hyperhomocysteinemia of alcoholics represents a risk factor for neurodegeneration that is potentially modifiable with pharmacological strategies of vitamin replenishment and total abstention from potus.