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Glutamate dehydrogenase (GLDH) catalyzes reversible deamination of glutamate into alpha-ketoglutarate and ammonium ion. In the metabolism of a cell, GLDH has the key role of acting as an interface between carbohydrates and amino acids in the vicinity of the citric acid cycle and urea cycle. In the brain, GLDH appears in astrocytic processes associated with glutamatergic terminals, but it is also involved in glia metabolic processes. GLDH probably protects postsynaptic membranes against the neuroexcitotoxic glutamate effect.

GLDH is an equally accurate marker of alcoholism in comparison to others, if its significantly faster decrease is taken into consideration. Watching changes in the activity of laboratory markers of alcoholism, after cessation of drinking, is an effective yet overlooked aid in diagnostics.

The fast increase of leukocytes GLDH activity is specific for alcohol addiction. Alcohol consumption reduces GLDH activity to some extent and consecutively it could lead to increased protein production and strengthen of diminished leukocyte protective ability.

The gradual decrease in GLDH activity may be one of key factors for neurodegenerative ageing processes. The decrease in GLDH activity in the cerebrospinal fluid of patients with neurodegenerative disorders may be one of the reasons for the neuroexcitotoxic glutamate effect.

The probable decrease in GLDH activity in the cerebrospinal fluid of patients with neurodegenerative disorders and of patients with nerve, nerve root and plexus disorders needs further investigations to be adequately understood.